About 70% of the population gets random muscle twitches. The medical term for this is fasciculation—spontaneous involuntary muscle contraction and relaxation. This could happen to your eyelid, arms, hands, fingers, legs, feet, or tongue.

There is even a medical condition called benign fasciculation syndrome. I believe this condition is really a nutritional deficiency. But, the typical treatment is cognitive behavioral therapy, anti-depression medication, and calcium channel blockers.

Random muscle twitches

In my opinion, random muscle twitches are caused by a magnesium deficiency. About 70% of the population also has a magnesium deficiency. Leafy greens are rich in magnesium.

Other symptoms of a magnesium deficiency: • Fatigue • Muscle cramps • Anxiety

Other potential causes of a muscle twitch: • High calcium • Low vitamin D • Alkalosis (potentially caused by a high carb diet or low potassium)

These are some of the most commonly known benefits of magnesium:

1. Leg cramps
2. Relaxation & calmness
3. Sleep
4. Inflammation
5. Blood sugar
6. Electrolyte
7. Bone health
8. Energy (ATP)

However, the real reason magnesium is essential is that it promotes a healthy heart and arteries.

The FDA allows the following health claim: “Consuming diets with adequate magnesium may reduce the risk of high blood pressure. However, the FDA has concluded that the evidence is inconsistent and inconclusive.”

Magnesium has a significant effect on the cardiovascular system. However, it’s also important that you consume a healthy diet. Taking magnesium won’t make much of a difference if you’re eating an unhealthy, carb-loaded diet.

Magnesium deficiency can have some potentially dangerous side effects, including: • Apathy • Depression • Convulsions • Cramps • Weakness

66% of the population does not meet the minimum requirement for magnesium. Magnesium levels have dropped significantly over the last 50 years.

The best sources of magnesium are vegetables. The average person only consumes 1.5 cups of vegetables each day—but you need 7 to 10 cups of vegetables daily for optimal health.

Other sources of magnesium include: • Grains (avoid!) • Green vegetables • Nuts and seeds • Seafood • Meats • Berries

Avoid these forms of magnesium supplements: • Oxide • Hydroxide • Carbonate • Sulfate

Stick with these forms of magnesium: • Citrate (may act as a laxative) • Threonate • Bisglycinate • Orotate • Taurate • Malate

• Taurate: heart and blood pressure
• Threonate: brain and memory
• Glycinate: relaxation and sleep
• Lactate: digestion
• Malate: energy and fatigue
• Chloride: blood sugar and digestion
• Orotate: heart
• Sulfate: muscle soreness

For constipation, bloating, IBS:

• oxide
• sulfate
• citrate

Start with 500mg going to 750mg or 1000mg, before bedtime Most people are low on magnesium in NA

Magnesium citrate - Absorbs easily. This can potentially be good for: • Nocturnal leg cramps • Constipation • Preventing headaches

Magnesium glycinate - Absorbs easily _ No laxative effects. This can potentially be good for: • Promoting a sense of calm • Supporting sleep • Reducing anxiety • Reducing inflammation • Supporting the blood sugars

Magnesium threonate - Best for the brain This can potentially be good for: • Improving cognitive function • Preventing the loss of synapses (in animal studies)

Magnesium orotate - Good for top athletes This can potentially be good for: • Improving energy • Supporting the mitochondria

Magnesium taurate This can potentially be good for: • Supporting the blood sugars • Supporting blood pressure (in animal studies)

Magnesium malate

• Laxative effect is small to none This can potentially be good for: • Fibromyalgia • Chronic fatigue syndrome

You may want to avoid these versions of magnesium: • Magnesium sulfate • Magnesium carbonate • Magnesium oxide • Magnesium hydroxide

Vitamins that support the absorption of magnesium • Vitamin D • Vitamin B6

There is no evidence to support the claim that most calcifying marine species will become extinct owing to higher levels of CO2 in the atmosphere and lower pH in the oceans. Claims about ocean acidification are unsupported by observational data.

The claim that the oceans are acidifying is unsupported

It is widely stated in the literature that the pH of the oceans was 8.2 before industrialization (1750) and that owing to human CO2 emissions it has since dropped to 8.1.25 No one measured the pH of ocean water in 1750. The concept of pH was not conceived of until 1909, and an accurate pH meter was not available until 1924. The assertion that more than 250 years ago ocean pH was 8.2 is an estimate rather than an actual measurement.

Oceans have powerful buffering capacity

The salt content of seawater provides it with a powerful buffering capacity, the ability to resist change in pH when an acidic or basic compound is added to the water. For example, one micromole of hydrochloric acid added to one kilo of distilled water at pH 7.0 (neutral) causes the pH to drop to nearly 6.0. If the same amount of hydrochloric acid is added to seawater at pH 7, the resulting pH is 6.997, a change of only 0.003 of a pH unit. Thus, seawater has approximately 330 times the buffering capacity of freshwater.23

Oceans less sensitive to CO2 increases

In addition to the buffering capacity, there is another factor, the Revelle factor, named after Roger Revelle, former director of the Scripps Institute of Oceanography. The Revelle factor determines that if atmospheric CO2 is doubled, the dissolved CO2 in the ocean will only rise by 10 per cent.

Oceans have wide pH fluctuations on a constantly changing basis

The pH of the oceans varies far more than 0.1 on a daily, monthly, annual and geographic basis. In the offshore oceans, pH typically varies geographically from 7.5 to 8.4, or 0.9 of a pH unit. A study in offshore California shows that pH can vary by 1.43 of a pH unit on a monthly basis.29 This is nearly five times the change in pH that computer models forecast during the next 85 years to 2100. In coastal areas that are influenced by run-off from the land, pH can be as low as 6.0 and as high as 9.0.

A warming ocean loses CO2 as it warms

What we do know is that if the oceans warm as the proponents of human-caused global warming say they will, the oceans will tend to release CO2 into the atmosphere because warm seawater at 30°C can dissolve only about half as much CO2 as cold seawater at 0°C does. This will be balanced against the tendency of increased atmospheric CO2 to result in more absorption of CO2 by the oceans. It does not appear as though anyone has done the calculation of the net effect of these two competing factors under varying circumstances.

Corals are resilient to changes in pH

A recent study published in the Proceedings of the National Academy of Sciences highlights how resilient coral reefs are to changes in ocean pH. A five-year study of the Bermuda coral reef shows that during spurts in growth and calcification, the seawater around the reef undergoes a rapid reduction in pH.48 This reduction in pH is clearly not causing a negative reaction from the reef, as it is associated with rapid growth.

A .3 pH reduction would have beneficial results among marine calcifying species (calcification, metabolism, growth, fertility and survival)

A review of these many studies, all of which use direct observation of measured parameters, indicates that the overall predicted effect of increased CO2 on marine species would be positive rather than negative

“Model Data” is being used instead of “Observational Data”

Members of the global science and lay communities have begun to learn of the confirmed omission of 80 years of instrumental data from contemporary ocean acidification (OA) scientific products. The missing ~2 million data points comprise a majority of the world’s historical ocean pH measurements. The data was replaced without disclosure, by a model hind cast. The substituted history, known as the FEEL2899 report (1) was itself used as the technical basis for testimony to the US Congress (2). In turn, OA mitigation research funding was augmented, and the regulation of anthropogenic greenhouse gas (GHG) emissions was strengthened and deepened.

https://wattsupwiththat.com/2015/03/31/ocean-ph-accuracy-arguments-challenged-with-80-years-of-instrumental-data/

Chemotherapy

Peter C Gøtzsche https://www.scientificfreedom.dk/2023/02/04/should-i-get-chemotherapy-for-cancer-probably-not/

Aspirin Use With Mortality Risk

Association of Aspirin Use With Mortality Risk Among Older Adult Participants in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6902761/

Benefits of vitamin C in cancer treatment.

Dr. Nathan Goodyear (https://twitter.com/drgoodyear)

90 percent of morbidity and mortality associated with cancer is when it spreads... Maximum tolerated chemotherapy actually induces the mechanisms to spread the cancer. In breast cancer, maximum to tolerated chemotherapy will reduce the primary tumor, yet at the same time, cause it to spread to distant locations in the body.

They really have two very different purposes. Whole food vitamin C is not suitable for the treatment of cancer, but does wonders for general health support, as it interacts favorably with copper and iron in your cells and mitochondria. I only recommend and use high-dose IV vitamin C in cases of acute infection or illness, as it does have very potent “drug-like” effects

“The point here is that vitamin C is not just directly killing cancer cells, what we would call cytotoxic effects. Vitamin C is actually working to change the metabolism of the cancer.

“What that means is, it creates an energy crisis. It actually depletes the body of certain intermediates that make it so this cancer, which is addicted to sugar, cannot use the sugar efficiently to make energy (ATP), so it … dies. It also depletes the cancer of its ability to detoxify.

“So, to be specific, research shows that vitamin C depletes the cancer of reduced glutathione. And getting rid of that glutathione in that cancer eliminates its ability to handle the high oxidative stress that this pro-oxidative vitamin C therapy induces, which kills the cancer cell.

https://www.theepochtimes.com/health/the-benefits-of-vitamin-c-in-cancer-treatment_5244645.html?utm_source=partner&utm_campaign=vigilantf&src_src=partner&src_cmp=vigilantf

Thomas N. Seyfried is Professor of Biology at Boston College, and received his Ph.D. in Genetics and Biochemistry.

He has over 200 peer-reviewed publications and is author of the book, Cancer as a Metabolic Disease: On the Origin, Management, and Prevention of Cancer. https://youtu.be/2Qd-Iyyek3Y

https://jessicar.substack.com/p/genotoxicity-and-carcinogenicity

Mechanistically, we found that the spike protein localizes in the nucleus and inhibits DNA damage repair by impeding key DNA repair protein BRCA1 and 53BP1 recruitment to the damage site.

Warburg effect

Cancer cells have dysfunctional mitochondria and cannot process energy properly. Because of this and their heightened energy demands they require 400 times the amount of glucose as regular cells. Limiting carbs limits energy to cancer cells.

Eczema is a condition where you have red, scaly, flaky, or rashy skin. This condition is also known as atopic dermatitis. Psoriasis is a part of the same family as eczema.

It is a Systemic disease - affects the whole body, inflammation Vascular associated disease because the ruptures, skin plaques are being fed by blood vessels - Angiogenisis. Many treatments just reduce the inflammation. Many people have sensitivity to gluten.

Traditional mediterrarean diet had lower severity.

• Extra virgin olive oil,
• hydroxytylenol (polyphenol found in olive fruits and olive leaves, a potent antioxident for the skin) (greek-koranectic, pql, moriola)
• seafood (Omega-3, flash frozen)

https://tomnikkola.com/hydroxytyrosol/

Gluten is almost always associated with the condition. Even evidence that removing oats, which doesn't have gluten, also promotes healing. So elimination diet time. Also celiacs are told to avoid corn.

Typical eczema treatments, like steroids, have potential side effects. So, we want to focus on natural alternatives for eczema.

This condition could be due to a deficiency of essential fatty acids caused by a poor diet or a genetic problem.

The #1 remedy for eczema: • Black currant seed oil (GLA)

What to do:

1. Take five drops of black currant seed oil and rub it in your hands to warm it up. Then apply it to the affected area.

2. Take a black currant seed oil supplement or a few drops with water orally.

https://e-journal.unair.ac.id/BHSJ/article/view/15007

https://www.sciencedirect.com/science/article/abs/pii/S0161589018305534?via%3Dihub

https://onlinelibrary.wiley.com/doi/10.1111/jdv.12033

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4690073/

https://pubmed.ncbi.nlm.nih.gov/20427696/

https://e-journal.unair.ac.id/BHSJ/article/view/15007

https://pubmed.ncbi.nlm.nih.gov/20545710/

https://ajcn.nutrition.org/

Glyphosate

Growing evidence that it is Glyphosate, the herbicide used in wheat crops, not actually gluten.

https://pubmed.ncbi.nlm.nih.gov/37196884/

https://denisrancourt.ca/uploads_entries/1627065545555_2021-07-DGR-comments-to-Health-Canada-re-Glyphosate-4.pdf

https://www.researchgate.net/publication/236211603_Glyphosate's_Suppression_of_Cytochrome_P450_Enzymes_and_Amino_Acid_Biosynthesis_by_the_Gut_Microbiome_Pathways_to_Modern_Diseases

https://www.researchgate.net/publication/261189254_Glyphosate_pathways_to_modern_diseases_II_Celiac_sprue_and_gluten_intolerance

Cod liver oil is the best remedy for nearly all skin conditions—especially eczema. Cod liver oil contains three powerful nutrients:

1. Omega-3 fatty acids (DHA and EPA)

2. Vitamin A

3. Vitamin D

One common symptom of low vitamin A is follicular hyperkeratosis. This is a condition where you have small brown or red hair follicles on your arms and/or back. Another symptom of low vitamin A is xerosis. This is when you have dried-out skin with fine wrinkles or a scaly appearance.

Vitamin A has a lot to do with the integrity of your skin—so it’s vital that you get plenty of it for your skin health.

Vitamin D is also vital for your skin health—especially psoriasis. Psoriasis is an autoimmune condition. Vitamin D is fantastic for all autoimmune problems. Vitamin D acts as a powerful anti-inflammatory—it’s like cortisol, but without the side effects.

Low levels of Omega-3 essential fatty acids can cause eczema. It’s important to increase your Omega-3 and lower your Omega-6.

Cod liver oil is rich in all of these important nutrients for your skin.

Many people on keto consume a lot of coconut oil and butter, which is great. However, these do not contain the Omega-3 you need. You need to consume sardines, salmon, or cod liver oil to get your Omega-3.

close gate.io account

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4690073/

https://onlinelibrary.wiley.com/doi/10.1111/jdv.12033

https://www.sciencedirect.com/science/article/abs/pii/S0161589018305534?via%3Dihub

https://e-journal.unair.ac.id/BHSJ/article/view/15007

https://pubmed.ncbi.nlm.nih.gov/20545710/

https://academic.oup.com/ajcn/article/70/4/536/4729115?login=false

The seasonal wave seems to be over in most places so it is time to revisit the numbers and see how our understanding has changed from our preliminary perspective on this pandemic. Remember, we were told that millions would die, and that we had to do our part to flatten the curve so that the health facilities would not be overrun. It was also just supposed to be for two weeks.

The average age of Canadians who died of COVID-19 in 2020 is 83.8 years, according to Statistics Canada, yet the Average life expectancy is only 76.5 years.

Excess deaths in Canada

Deaths in Canada for Covid-19 are reported to be 8,947 for the 18th month period ending Aug 5, 2020. 90% of those deaths were people 70 and older. 82% of deaths occurred in Long Term Health Care facilities. In the province of Quebec it was 93%. Annual deaths in Canada are approximately 300,000 so Covid-19 deaths are just under 3% of that.

Leading causes of Death, Canada 2018 (for 12 month period)

Rank	Cause of death	Total deaths
1	Cancer	79,536
2	Heart disease	53,134
3	Cerebrovascular diseases	13,480
4	Accidents	13,290
5	Chronic lower respiratory diseases	12,998
6	Flu and pneumonia	8,511
7	Diabetes	6,794
8	Alzheimer’s disease	6,429
9	Suicide	3,811
10	Kidney diseases	3,615

Lets look at all-cause mortality, as provided by StatsCan.

https://www150.statcan.gc.ca/n1/daily-quotidien/200724/dq200724a-eng.htm

https://www150.statcan.gc.ca/n1/pub/71-607-x/71-607-x2020017-eng.htm

The following graphs, taken from their website, show the number of deaths in each week for the past five years. For comparison, each year is superimposed over top of each other, and each year is represented by a different colour. The current year is represented by a dashed line.

Even though these graphs were just released, I have no explanation for why the covid period ends in May. I am going to assume it is just due to a processing delay of the raw information. This is my biggest problem with StatsCan - they are not transparent about what they are doing.

Looking first at children and young adults, we are unable to see anything unusual in this year compared to prior years. It is actually difficult to see the Covid period because it is right in the middle of previous years. There does not appear to be any excess deaths caused by COVID19 for this age group. Why are we involving children in this pandemic scare when they are no more affected by it than they would be by the seasonal flu.

Children and young adults

Adults

Deaths for adults is also lower than normal, which is actually quite surprising.

Senior Citizens

Only with the senior citizens do we see a noticeable but temporary increase in the number of deaths, followed by a decrease below normal level. So how will this average out over the year?

Elderly

Finally, looking at the elderly, we clearly see a bump in the number of deaths for a few weeks. Even then, April deaths are below January deaths, and as we have already seen, the rise above normal is followed by a fall below normal which means the year will average out as, well, average.

Just a reminder. The typical government response to the alarming rise in covid deaths at the beginning of the first wave was to draw down the number of patients in the hospitals by sending them back to the LTC's. A number of people have noted that this caused problems for the other residents of the LTC and resulted in a wave of additional deaths.

2024 UPDATE

Stats Canada now have an update to the graphics that were released back in 2020 that worth looking at.

Excess mortality in Ontario (2020)

Statscan has also provided graphs for all-cause mortality for a number of the provinces. Here is what Ontario looks like.

Ontario deaths in 2020-compared to previous 5 years

You can find it here. https://www150.statcan.gc.ca/n1/daily-quotidien/200724/g-a004-eng.htm

Sure there was a bump that began two weeks after the lockdowns (Mar 12) but it was short lived and compares similarly with the previous 5 years. It has all ages combined so once again, it is mostly those over 70. Also, from May onward, deaths are below normal compared to the previous 5 years.

US deaths as reported by the CDC

Majority of deaths occurred in Long Term Care Facilities

This is such an important point because the media and politicians try to portray the risk being equal across the population. But this is simply not the case. In Quebec, deaths in Long Term Care facilities accounted for 93% of deaths which is pretty much all of them. The remaining 7% were not in LTC but also had comorbidities, which means they were already dying of something else. Remember, 100% had at least one comorbidity. 99% had two or more. What most people do not realize, or may have forgotten is that people that go into Long Term Care Facilities are already sick and frail. The average lifespan of a resident in an LTC is 18 months. Which means the attrition rate is 30% of the population of the LTC, each year. In addition, deaths are very seasonal with half of them occuring during the flu season, which amounts to 15% of the population of the LTC. This is exactly the same death rate that occurred during the initial Covid outbreak. Most LTC's experienced about 15% of deaths. And remember, this is an average across all LTC's. Some had higher percentages and some had lower. 15% is the average. This is why we are saying Covid mortality is pretty much in keeping with influenza mortality and why StatsCan are not reporting any excess deaths.

How Canada compares to other countries

In terms of deaths per million, Canada ranks around 184 as shown by worldometers.info with 237 deaths per million. That means 183 countries did better than us. This puts us in the middle of it's peer of first world countries. (100-1000 deaths/million) which I have covered in another blog post. In comparison, USA ranks 205 with 479 deaths per million, more than twice Canada’s rate. Sweden, which I will get back to shortly, came in at 202, pretty close to Canada. A question that really needs to get answered is why are we in a cluster that is 10x - 100x more severe than countries that are in the single-digit cluster:

Clustering

cluster (deaths/million)	cohorts (sample)
100-1000	Belgium, Peru, Spain, Italy
10-100	Canada, US, Sweden, Norway, Netherlands
1-10	China, Singapore, Hong Kong, South Korea, Japan

We still have no explanation offered why the proportion of deaths varies so widely from one country to the next. Is it due to their methods of counting? Are they healthier? Do they have less old people?

The death rate for the Seasonal flu around .1% of those infected, which is called the IFR. With Covid19, we are seeing a 3.6% case fatality rate, which is referred to as CFR. However, cases refer only to those that have been tested, not to the overall population, which is something that is used in the seasonal flu calculations, so you can not compare those two numbers without making an adjustment to determine how many people were actually infected. You have to compare Covid IFR to Seasonal flue IFR if you want to do a comparison.

Canada has tested just over 10% of the population with 4.5 million tests out of a population of 37 million which resulted in 120 thousand cases. Could this be extrapolated to the whole population to derive an estimated 1 million cases? That would put the case death rate at .36 if it is true. Difficult to estimate the total number of those infected, but we do know most are asymptomatic so it is probably a high number.

The Covid19 pandemic can also be compared to the last three flu pandemics during the last century. But remember, the population has doubled a few times during this period so past events would have to be scaled up to as much as 3x to compare to today’s population, and these numbers have not been population adjusted. For example the 25-50 million deaths a hundred years ago would be equivalent to 75-150 million proportional deaths given hat the size of our current population has grown 3 times during that period.

• 1918 flu pandemic – 25-50 million deaths
• 1957 flu pandemic – 1-2 million deaths with death rate around .67
• 1968 flu pandemic – 1-4 million deaths. Immunity from 1957 carried forward
• 2020 Covid19 pandemic – 0.75 million deaths.

Note. When I first wrote this, Aug 2020 the first wave of deaths was over. Since then the mainstream media continues to report that as many as 50 million have died from covid. Is that actually true?

Children

Children are doing better in 2020 than previous years.

Here is an interesting graph from EUROMOMO for children all across Europe. 2020 is shown to be lower than the previous 5 years for this age group.

EUROMOMO: Deaths for children are lower than previous years in all of Europe

All Cause Mortality Canada Historic

All Cause Mortality (UPDATED Dec 2022)

USA experience (CDC)

https://data.cdc.gov/NCHS/Provisional-COVID-19-Death-Counts-by-Sex-Age-and-S/9bhg-hcku

https://journals.lww.com/pidj/Fulltext/2022/04000/The_Role_of_Children_and_Young_People_in_the.29.aspx

April, 2022 edition of The Pediatric Infectious Disease Journal, entitled, “The Role of Children and Young People in the Transmission of SARS-CoV-2,” concluded: “there is NO convincing evidence to date, 2 years into the pandemic, that children are key drivers of the pandemic.

Childhood covid-19 disease burden, however, is not exclusively defined by mortality; it includes morbidity. To that end, I have begun analyzing hospitalization datasets I purchased from RIDOH for all hospitalizations in our state, organized by what are called ICD diagnostic codes, for calendar years 2019, 2020, and 2021, comparing influenza and covid-19 hospitalizations among children, up to age 18. My initial analyses are summarized in the tables provided, below.

What is the evidence that masking of children in schools can reduce their risk for contracting and transmitting covid-19 regardless of their very low risk for clinically significant disease?

Notes and References

These are new items of interest for this topic that I have recently discovered but not yet explored.

death < 14 days

https://twitter.com/MartinNeil9/status/1466814347762671628

contrary argument on vaers

https://twitter.com/ENirenberg/status/1498852915758485509

C19 “vaccine” - the cause of causes

https://coquindechien.substack.com/p/c19-vaccine-the-cause-of-causes?s=r

New-onset autoimmune phenomena post-COVID-19 vaccination

https://onlinelibrary.wiley.com/doi/full/10.1111/imm.13443

US covid test positivity rates by vaccination status

yet another set of evidence that vaccines are not working to stop covid spread and that boosters wind up making you more likely to contract covid in the long run

https://boriquagato.substack.com/p/us-covid-test-positivity-rates-by?s=r

Myocarditis, Pulmonary Hemorrhage, and Extensive Myositis with Rhabdomyolysis 12 Days After First Dose of Pfizer-BioNTech BNT162b2 mRNA COVID-19 Vaccine: A Case Report

(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8865877/)

Case Report: Anti-NF186+ CIDP After Receiving the Inactivated Vaccine for Coronavirus Disease (COVID-19) chronic inflammatory demyelinating polyneuropathy (CIDP)

https://www.frontiersin.org/articles/10.3389/fneur.2022.838222/full

A Case Series of Ketoacidosis After Coronavirus Disease 2019 Vaccination in Patients With Type 1 Diabetes

https://www.frontiersin.org/articles/10.3389/fendo.2022.840580/full

https://twitter.com/DrJohnB2

A Public Health Emergency in Canada: The Rate of Change in Excess Millennial Deaths Can’t Be Explained by a Sudden Rush of Suicides, Overdoses, Cancers

https://lionessofjudah.substack.com/p/a-public-health-emergency-in-canada?s=r

Something is not right

Like everyone else, I have had my series of childhood vaccinations and never thought much about it. At least until now. But, there is something about these new Covid vaccines that does not seem right. They appeared awfully fast, just months after a novel virus appears. They are not even vaccine's in the traditional sense: neutered virus particles that are meant to stimulate an immune reaction to the pathogen without the ability to replicate. Nor are they something that has ever been used on humans before. We should have proceeded with caution. We should have followed the safety protocols of clinical trials. The system failed us.

Clinical trials are underway and will not be reporting their results until 2024. I have already published a blog on this What is a Clinical Trial? The key thing to know about the clinical trials is that they are a protocol developed after decades of trial and error. It is the best way and safest way that we know in order to get new drugs to market. Tampering with this should never have occurred. Furthermore, the pharmaceutical companies were offered immunity from prosecution and civil litigation. The latest is that the pharmaceuticals have now been given permission to adjust the recipes for their vaccines without going back through clinical trials. All our protections have been removed. Why are people ok with this?

USA Adverse Reporting

The USA maintains a Vaccine Adverse Event Reporting System (VAERS) that can be found here. https://vaers.hhs.gov/

European Adverse Reporting

Europe maintains their own adverse reporting and can be found here. https://dap.ema.europa.eu/analytics/saw.dll?PortalPages

Canadian Adverse Reporting

There is an adverse reporting system in Canada, and can be found here. https://health-infobase.canada.ca/covid-19/vaccine-safety/

The following was taken from Canada’s reporting system on Feb 10, 2021.

Of the 480 individual AEFI reports (0.051% of all doses administered), 68 were considered serious (0.007% of all doses administered). The 480 individual adverse events reports represent 480 people who reported one or more adverse events. Among the 480 adverse events reports, the most frequently reported adverse events were:

• vaccination site reactions,
• paraesthesia (tingling or prickling),
• urticaria (hives),
• pruritis (itching), and
• nausea.

Among the 68 serious adverse events reports, the most frequently reported adverse event was anaphylaxis.

Three deaths were reported. These deaths occurred after the administration of a vaccine. Following medical case review, it has been determined that these deaths are not linked to a COVID-19 vaccine.

There may be delays in receiving reporting forms. These delays may be due to jurisdictions investigating and reviewing each AEFI prior to submitting the information to PHAC. There are also limitations to reporting practices such as under reporting, missing information, and differing AEFI reporting practices across jurisdictions in Canada. Information is collected on individuals for whom an AEFI report was submitted, not on the total number of individuals who experience an adverse event as not every adverse event is reported.

Does it work?

Again, very difficult to assess this because clinical trials are underway but not yet reporting. They claim the vaccines are effective, but they needed to make this claim to get regulatory fast track approval. They are relying on the outcome of the clinical trials that are underway to prove this claim. It is not yet proven. I have had this argument with a number of people. The pretrials did not prove effectiveness against death or hospitalizations. That is a false assumption that everyone seems to make. They define effectiveness as measured by counting the number of symptoms, which is highly subjective, vague and inconclusive.

Do I need it?

This one is easy to decide. In Canada, according to StatsCan, 80% of deaths are people in their 80’s. 82% are in long term health care facilities (93% in Quebec). 99% have comorbidities. None of these factors apply to me, so if anything, I am in the other group – the 10% of deaths who are under 70. On further consideration, the age is an issue for comorbiditie more than covid outcome. The table on CFR by age is a better measure. But remember, CFR is a measure of people seeking medical assistance not an actual measurement of people getting sick.

But again, 99% of those are with comorbidity, leaving me in the 1% of the 10%. That is pretty good odds in my favour, should I actually encounter the virus.

Dataset: Ontario #COVID19 age-stratified CFRs

Dataset: Ontario deaths by vaccination status

age range	CFR	Rate
0-19:	0.003%	(1 in 32,018 cases)
20-29:	0.008%	(1 in 12,075)
30-39:	0.03%	(1 in 3,542)
40-49:	0.076%	(1 in 1,316)
50-59:	0.30%	(1 in 329)
60-69:	1.43%	(1 in 70)
70-79:	3.64%	(1 in 27)
80-89:	10.96%	(1 in 9)
90+:	19.31%	(1 in 5)

So because I do not have comorbidity, my odds are much greater than 1 in 70 and may even be closer to 1 in 7000 but certainly at least 1 in 700.

age range	IFR
0-19	.0013%
20-29	.0088%
30-39	.021 %
40-49	.042%
50-59	.14%
60-69	.65%
70+ nonLTC	2.9%
70+ all	4.9%

The odds are also pretty good that I won’t even encounter the virus this year. I just checked the Covid-19 case tracker for Canada and after a year, we seem to have about 804,000 cases. Out of 38 million Canadians, that is about 2.1% of the population, or 1 in 47, so my chance of getting Covid in the next year is probably the same as last year which is 1 in 47. Again, pretty low odds. So why take a risky procedure for something that I have very low odds of getting and very low odds of perishing if I get it. I can afford to wait a few years and watch what happens, and make a more informed decision at that time.

So, to summarize, 2.1% chance of getting Covid and a 1.43% chance of perishing if I get Covid leaves me with a 0.03% chance of perishing from Covid this year. Compare that with a 100% chance of perishing in the next 30 years or 3% chance per year (an actuarial table gives it at 2% because your chance of dying doubles every 8 years).

ex Chief Scientific Officer for Pfizer (Mike Yeadon) is risking his career and reputation to warn people that they will eventually create a mass casualty event, people should prob heed his warning.

professor and Viral immunologist Dr. Byram Bridle, - the spike protein is a toxin that should not be deployed en masse

Pathologist Dr. Roger Hodkinson -they are lying about everything.

Dr. Peter McCollough is risking his career, - the jabs are ineffective and mandating them is useless.

Dr. Patrick Philips - damages caused by lockdowns and suppression of treatments.

[“These vaccines don’t prevent transmission.. Infections can still happen whether ppl vaccinated or not.. This idea that vac mandates needed to create safe workplaces is a complete lie & is not backed by science.. Denial of natural immunity”](FL Surgeon General, Twitter account removed)

Discussion and Summary

The scientific methods states that any claim can be made but it has to be observable and repeatable to be proven. It also has the concept of a null hypothesis, in that one would have to show the efficacy of a

Bananas are a healthy source of fiber, potassium, vitamin B6, vitamin C, and various antioxidants and phytonutrients.

• Vitamin B6 (33% DV)
• Fiber (10% DV)
• Potassium - 0.4g 422mg
• Magnesium (8% DV) 32mb
• Vitamin C (10% DV) 10mg
• Manganese
• Vitamin A

Resistant starch and pectins act as prebiotic nutrients, supporting the growth of beneficial gut bacteria.

Improving insulin sensitivity, promoting weight loss, and reducing some of the liver and kidney issues associated with diabetes.

Bananas are a good source of prebiotics, the fermentable fibers that help feed "good bacteria," or probiotics, in the gut. Prebiotics aid digestion by promoting the growth of bacteria that help digest food. Pairing bananas with foods that contain live cultures (such as yogurt) is a great way to support gut health, digestion, and regularity.

Blueberries. You should probably eat more of them. They're high in polyphenols, flavinoids, and anthocyanin . All of these improve blood flow. (flavinoids also boost BDNF, which is essential for growing new neurons)

One serving - one cup (148g),

• Calories: 84
• Fat: 0.5g
• Sodium: 1.5mg
• Carbohydrates: 21g
• Fiber: 3.6g
• Sugars: 15g
• Protein: 1g
• Vitamin C: 14.4mg
• Vitamin E: 0.8mg
• Vitamin K: 28.6mcg
• Vitamin B6: 0.1mg

Glycemic load is below 10, which is considered low.

Vitamins and Minerals

Blueberries are a rich source of essential nutrients, including vitamin C, vitamin K, and the mineral manganese, which helps the body process cholesterol and nutrients like carbohydrates and protein. Vitamin K is a key nutrient in blood clotting and healthy bones.

Health Benefits

Blueberries contain compounds known as polyphenols, which are sort of an all-around star for good health. Scientists have found many benefits to blueberries due to the micronutrients they provide. There are studies that show eating 1/3 cup of blueberries daily is associated with reduced risk of disease.

Improved Memory

Blueberries have been shown to help maintain memory and prevent cognitive decline. One small study showed that people who regularly drank blueberry juice had improved performance on memory tests (and also decreased symptoms of depression). A much larger, long-term study, published in 2012, credited berries for delaying cognitive aging by as much as two and a half years.

Fight Inflammation

Phyto (plant) components are abundant in blueberries. These include flavonoids, which are responsible for the berry's antioxidant and anti-inflammatory activities. Blueberries also have lots of vitamin C. It acts as an antioxidant, aiding in wound healing, supporting the immune system, and providing anti-aging properties.

Reduce Heart Attack Risk

In one study, eating three or more weekly servings of berries like blueberries reduced the risk of heart attack in women by 32%.7 Blueberries are so beneficial in part because they're rich in heart-healthy, filling fiber. Fiber is the indigestible part of carbohydrate that aids in satiety, regulates the bowels, helps pull cholesterol away from the heart, and helps stabilize blood sugar.

Blueberries also contain anthocyanins, antioxidants that may benefit the heart by improving blood flow and countering plaque buildup.

Decrease Cancer Risk

Some research suggests that eating foods with anthocyanins may also help to fend off cancer.9 Anthocyanins are a type of flavonoid, and they are found in brightly colored fruits and vegetables including blueberries.

Improve Insulin Sensitivity

Although blueberries do contain naturally occurring sugars, their anthocyanins appear to improve insulin sensitivity and help lower blood sugar levels. That means they can help lower the risk of insulin resistance and type 2 diabetes.

References

Kimble R, Keane KM, Lodge JK, Howatson G. Dietary intake of anthocyanins and risk of cardiovascular disease: A systematic review and meta-analysis of prospective cohort studies. Crit Rev Food Sci Nutr. 2019;59(18):3032-3043. doi:10.1080/10408398.2018.1509835

Institute of Medicine (US) Panel on Micronutrients. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington (DC): National Academies Press (US); 2001. 10, Manganese.

Kalt W, Cassidy A, Howard LR, et al. Recent research on the health benefits of blueberries and their anthocyanins. Adv Nutr. 2020;11(2):224-236. doi:10.1093/advances/nmz065

Krikorian R, Shidler MD, Nash TA, et al. Blueberry supplementation improves memory in older adults. J Agric Food Chem. 2010;58(7):3996-4000. doi:10.1021/jf9029332

Devore EE, Kang JH, Breteler MM, Grodstein F. Dietary intakes of berries and flavonoids in relation to cognitive decline. Ann Neurol. 2012;72(1):135-43. doi:10.1002/ana.23594

Carlsen MH, Halvorsen BL, Holte K, et al. The total antioxidant content of more than 3100 foods, beverages, spices, herbs and supplements used worldwide. Nutr J. 2010;9:3. doi:10.1186/1475-2891-9-3

Cassidy A, Mukamal KJ, Liu L, et al. High anthocyanin intake is associated with a reduced risk of myocardial infarction in young and middle-aged women. Circulation. 2013;127(2):188-96. doi:10.1161/CIRCULATIONAHA.112.122408

Kimble R, Keane KM, Lodge JK, Howatson G. Dietary intake of anthocyanins and risk of cardiovascular disease: A systematic review and meta-analysis of prospective cohort studies. Crit Rev Food Sci Nutr. 2019;59(18):3032-3043. doi:10.1080/10408398.2018.1509835

Yousuf B, Gul K, Wani AA, Singh P. Health benefits of anthocyanins and their encapsulation for potential use in food systems: a review. Crit Rev Food Sci Nutr. 2016;56(13):2223-30. doi:10.1080/10408398.2013.805316

Martineau LC, Couture A, Spoor D, et al. Anti-diabetic properties of the Canadian lowbush blueberry Vaccinium angustifolium Ait. Phytomedicine. 2006;13(9-10):612-23. doi:10.1016/j.phymed.2006.08.005

Stull AJ, Cash KC, Johnson WD, Champagne CM, Cefalu WT. Bioactives in blueberries improve insulin sensitivity in obese, insulin-resistant men and women. J Nutr. 2010;140(10):1764-8. doi:10.3945/jn.110.125336

Cunningham E. Are there foods that should be avoided if a patient is sensitive to salicylates?. J Am Diet Assoc. 2010;110(6):976. doi:10.1016/j.jada.2010.04.020

Rane A, Lindh JD. Pharmacogenetics of anticoagulants. Hum Genomics Proteomics. 2010;2010:754919. doi:10.4061/2010/754919

Bouzari A, Holstege D, Barrett DM. Mineral, fiber, and total phenolic retention in eight fruits and vegetables: a comparison of refrigerated and frozen storage. J Agric Food Chem. 2015;63(3):951-6. doi:10.1021/jf504890k

Milk Benefits

Milk has very little natural trans fat. You can measure it in milk. Some saturated fat will be trans fat but it is exceedingly small and for the most part not to be worried about. If it's real food. Really, trans fat is a synthetic phenomenon that the food industry puts in specifically to increase shelf life. so I think that we can ignore the inherent trans fat in real food and focus on just what the industry does to you know sale to sell their uh their products and that's what the FDA is worried about .

Let's stick on that milk piece because this isn't a really important interesting fact about saturated fat that not a lot of people are talking about the fact that there's two different kinds and you mentioned in red meat there's a type that's basically neutral

Within milk or dairy there's the saturated fat that has possibly even a little bit of a benefit because it's anti-inflammatory potentially. This is a little complicated. Milk generates an enormous amount of visceral reaction so let me unpack it

Let me take it apart for you there are some people who are intolerant to lactose. okay full stop you know stay away from it. There are some people who are intolerant to certain milk proteins and develop milk protein allergy. stay away from it.

If you consume milk and you end up having enormous GI side effects okay that's probably a problem. If that's true what you should try to do is you should try to take some lactate so you know lactase as a as a supplement and see whether or not you still have it if you still do just stay away from it that is probably the you know those two things lactose intolerance and milk protein allergy is probably about 20 percent of the population so not insignificant or a lot of people.

African-Americans have you know significant increase risk of lactose intolerance. Jews have an increased uh risk of lactose intolerance but that can be mitigated by taking lactase by mouth. By the way I do that's how I consume Dairy is with um uh lactate okay because I'm Jewish the way it is. About the rest of us is there something in milk that's worthwhile.

• Number one there's lots of amino acids and that's good.
• Number two there's lots of fatty acids including some essential fatty acids, so that's good.
• number three there's a lot of calcium

Calcium

Here's the problem with the calcium story. Everyone says you need calcium. You do you absolutely do, no question. Calcium for bones. Calcium for muscle functioning. Calcium for hormone release. Calcium is essential and milk is a very good source of calcium so you would say well then you should drink milk because of the calcium and we tell postmenopausal women to drink milk because of the calcium. We are given vitamin D too right. Wrong this is the mistake and the reason is not because there's not calcium there is but because there's way more phosphorus in milk in order to absorb calcium you have to have a calcium phosphate product that is conducive to absorption and the problem is that the phosphorus the phosphate binds the calcium so it becomes calcium phosphate or calcium biphosphate or diphosphate and makes it unavailable for absorption so in other words in order to absorb calcium you have to have calcium without phosphate and that's not milk that's other foods but it's not milk so in fact the calcium that's in milk is for the most part unabsorbable and that's one of the reasons why giving milk to people with osteoporosis doesn't seem to benefit them in fact might even hurt them

now can you give calcium pills yes you can get calcium pills but does that fix osteoporosis no that doesn't fix osteoporosis either and the reason is because the calcium just gets absorbed and goes right through you does not end up in the bone you have to do some things to the Bone in order to get that calcium into the bone and unfortunately vitamin D is not the answer to that that's why all of these trials of calcium and vitamin D in post-menopausal women have failed so the notion that you can actually reverse osteoporosis by drinking milk which is of course you know this you know Common Urban myths that's out there you know does not work as a pediatric endocrinologist I used to take care of multiple children with hypocalcemia low serum calcium levels and look these these kids sick you know the George syndrome or congenital hypoparathyroidism or autoimmune hypoparathyroidism or you know host of different diseases leading to hypocalcemia we had to boost these kids serum calcium levels to keep them from having seizures and tetany and you know and stopping of the heart and what have you okay you know this is a big deal in order to do that we had to give them calcium and we had to make sure that the calcium was absorbed so we actually had to take away the milk we had to take away Dairy we had to give the calcium with no phosphorus we had to increase the calcium to phosphate product in the in in whatever they were eating to four to one four calciums to one phosphorus whereas milk is one to two one calcium to two phosphoruses so we actually had to take away the milk and give them calcium without phosphorus we had to give them calcium supplementation in the form of calcium globionate or calcium chloride or something else very specifically to increase the absorption so this notion that milk is important because it has calcium is actually not correct in addition milk does not have vitamin D in it until or unless you irradiated so standard stored bought milk will be irradiated and that's how it has high vitamin D so you can buy unvitamin D milk you know if you buy it from a local farmer or whatever but that is not a good method for supplementing your vitamin D so there are all sorts of issues with respect to milk and then finally

cancer from milk myth

let me address one last myth about milk and that is that it causes cancer and this all came from one book and that book is called The China Study written by Campbell and ezelstein. what they did was they looked at the population of China and they did an epidemiologic analysis 500 pages of single univariate correlations and base you know and snapshot in time no no uh time component in in the analysis and what they came up with was that the consumption of dairy correlated with increased incidence of cancer and so they said therefore milk causes cancer and they said the casein the protein in milk uh you know the primary approaching milk was the bad guy um number one this is not how you determine causation uh univariate correlations are not the same as multivariate correlations and multivariate correlations are not the same as causation in order to determine this you'd have to have a Time component which they do not have okay and also you know there's this thing called reverse causation you know where it might be actually people with cancer might have you know altered you know food intake and it might also be that um there's intermediate causation something else is causing both of those things that has nothing to do like for instance ice cream consumption correlates with drownings is it that ice cream causes drownings or is it that survivors of drownings you know bury their heads in a banana split well neither okay you know um ice cream usually is consumed when it's hot outside people swim when it's hot outside and some people who swim drown okay so yes ice cream consumption is correlated with drownings having nothing to do with any causation linking those two things directly rather there's an antecedent that leads to both of those separately that's called an Epi phenomenon so it very well may be that you know what they what they were studying in China was an Epi phenomenon not a primary cause of a phenomenon there's no data that suggests that drinking milk increases aristocrification let's stick on The China Study here for a little bit that book seems to have a lot of legs and continues to get broughten up time and time again and the reason I want to stick with it is there any data that they gain from that study that we can use or because of the variables that you talked about there and the way it was done there's there's no there's only associations made and there's nothing we can really take from it there's only Association and you know there's a lot of mumbo-jumbo in nutrition based on Association and nutrition has been derided by multiple scientists as being basically the dark arts of medicine and to be honest with you if you use it wrong they're right they're correct John ianidis of Stanford who is you know perhaps the biggest statistical Guru you know you know alive today in terms of how to interpret data basically says we should stop all nutrition research because it's all um now I think that's a little severe personally although you are trying to kill the word nutrition I'm trying to kill the word calorie okay I thought it was nutrition as well no I'm not trying to kill the word nutrition I'm trying to put in its proper place got it so actually let's go there for a minute we I think we've beaten calcium and milk to it you know to Smithereens

Benefits

Health Benefits - Oatmeal is nutritionally rich. It has more protein than most grains and also contains numerous vitamins and minerals. It contains antioxidants and a soluble fiber called beta-glucan, which aids several systems of the body. Oatmeal provides many health benefits, including these:

Gut Health - The beta-glucan soluble fiber promotes regular emptying of the bowel and prevents constipation. It also supports healthy gut bacteria, which may reduce the symptoms of irritable bowel syndrome and other intestinal problems.

Lower Cholesterol - Soluble fiber like the beta-glucan in oatmeal lowers cholesterol. In one study, those who ate oat bran experienced a 23% drop in total cholesterol. Researchers believe that several mechanisms in the body are responsible for the lower cholesterol.

Heart Health - Oats are high in antioxidants called avenanthramides, not found in other cereal grains. These antioxidants reduce inflammation and relax arteries, improving heart health.

Blood Sugar Control - The soluble fiber in certain oats can keep blood sugar from rising after a meal. The glycemic load of less-processed oats is low to medium, making them a suitable carbohydrate for those with diabetes. Those who have diabetes should avoid instant oatmeal, which has a high glycemic index.

Weight Control - Eating fiber-rich foods like oatmeal produces a feeling of satisfaction, which can make it less likely that you will overeat. The particular fiber in oatmeal, beta-glucan, makes the contents of the intestines very viscous and may make you feel full longer.

Nutrition

Oatmeal is high in several vitamins and minerals:

• Manganese
• Molybdenum
• Phosphorus
• Copper
• Biotin
• Vitamin B1 (Thiamine)

Usage suggestions

• Add oatmeal instead of bread crumbs to meatloaf or burgers.
• Enjoy a meatless meal by making a lentil loaf with oats.
• Make oatmeal cookies instead of less-healthy sweets.
• Try simple savory oats by topping oatmeal with soy sauce and green onions.
• Make overnight oats and snack on them anytime you get hungry.
• Create your own granola with oats, nuts, and dried fruit.
• Add oatmeal to plain yogurt along with unsweetened fruit for a healthy breakfast or snack.
• Make a crisp by topping fruit with a mixture of flour, oats, and sugar.
• Add oats to pancake batter. For a smoother texture, whir them in a food processor first.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4690088/

https://www.ewg.org/news-insights/news-release/ewg-responds-general-mills-and-quaker-oats-legal-not-same-safe

https://www.ewg.org/news-insights/news/glyphosate-contamination-food-goes-far-beyond-oat-products

https://www.ewg.org/research/ewg-investigation-dangerous-agricultural-chemical-chlormequat-found-popular-oat-based

https://pubmed.ncbi.nlm.nih.gov/21294744/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3524229/

https://pubmed.ncbi.nlm.nih.gov/21843037/

• Vitamin A = immunity (viruses), eye health, helps iodine absorption

• Vitamin B1-B3 = energy

• Vitamin B5 + B6 = neurotransmitters

• Vitamin B7 = hair & nails

• Vitamin B12 = blood cells

• Vitamin C = collagen

• Vitamin D = Bone, immune, Blood Pressure, Pain - made by your skin, helps calcium absorption

• Vitamin E = antioxidant, neurological, muscle, heart, arteries,

• Vitamin K1 = Clotting, DNA

• Vitamin K2 = arteries, Calcium transport

• Inositol = Sleep

• L-theanine = Calm

• Magnesium = Relax

• B-Complex = Energy

• Vitamin D3 = Immunity

• Chromium = Blood sugar

• Vitamin K2 = Heart health

• Blackseed oil = Immunity

• Cod liver oil = Allergies

• Creatine = Muscle

• Collagen = Joints

• Fish oil = Inflammation

Earliest signs of nutritional deficiencies

1. Vitamin A - Difficulty seeing in the dark

2. Vitamin B1 - Nervous tension

3. Vitamin C - Swollen or red gums with slight bleeding

4. Vitamin D - Bone pain

5. Vitamin E - Muscle weakness

6. Vitamin K1 - Excessive bruising

7. Vitamin K2 - Tartar buildup

8. Calcium - Chronic cough

9. Iodine - Breast tenderness

10. Sodium - Overall weakness

11. Magnesium - Loss of energy

12. Potassium - Pounding in your ears when trying to sleep

13. Selenium - Brain fog

14. Zinc - Getting out of breath upon exertion

98% of vitamins are synthetic, and most come from china and have questionable regulation and they use petroleum products. Therefore, Supplements should not be taken on a regular basis for health but periodic detox is ok. Supplements have traces of industrial chemicals chloroform, petroleum, methonal, formic acid, Toulene, herbicides, hexane and none of these are found in nature

Best source of vitamins are from food.

Microbes in gut make some of the vitamins.

Bio-availability is lost when using supplements. Shown in numerous clinical trials.

Nature makes sure these are grouped together to better deal with free radicals.

Vit-c decreases muscle mitochondria and muscle training efficiency.

Retinol - best form of Vit-A

Beta-Carotene- unfortunately only a tiny bit of Vit-A gets absorbed

https://chrismasterjohnphd.com/blog/2019/03/06/vitamins-minerals-101

Vitamins to take as you get older

• Vitamin C - loser histamine, help with cancer
• Vitamin B3 Niacin - 500-1000mg
• Magnesium
• Vitamin D - 10,000 iU
• Vitamin K1
• Vitamin K2 energy

B complex vitamins

https://www.healthline.com/nutrition/vitamin-b-foods#TOC_TITLE_HDR_5

Many foods are high in B vitamins, including certain types of meat, fish, and poultry, legumes, seeds, eggs, dairy products, and leafy greens.

Some top sources of B vitamins include meat (especially liver), seafood, poultry, eggs, dairy products, legumes, leafy greens, seeds, and fortified foods, such as breakfast cereal and nutritional yeast.

If you restrict your intake from some food groups due to allergies or diet, your chances of B vitamin deficiencies may increase.

Produce energy and make important molecules. All, except B12 are short-lived.

• thiamine (B1)
• riboflavin (B2)
• niacin (B3)
• pantothenic acid (B5)
• pyridoxine (B6)
• biotin (B7)
• folate (B9)
• cobalamin (B12)

Salmon 3.5(oz)/ 100(g)

• Thiamine (B1): 23% of the Daily Value (DV)

• Riboflavin (B2): 37% of the DV

• Niacin (B3): 63% of the DV

• Pantothenic acid (B5): 38% of the DV

• Pyridoxine (B6): 56% of the DV

• Cobalamin (B12): 127% of the DV

• high in beneficial omega-3 fats

• protein

• elenium

Leafy greens - folate (B9)

• Spinach, raw: 12% of the DV in 1 cup (25 g)
• Spinach, cooked: 39% of the DV in a 1/2 cup (90 g)
• Collard greens, cooked: 17% of the DV in 1/2 cup (65 g)
• Turnip greens, cooked: 21% of the DV in 1/2 cup (73 g)
• Romaine lettuce, raw: 3% of the DV in 1 cup (35 g)

Minimize folate loss during cooking, steam the greens until partway between tender and crisp.

Beef Liver 3.5-oz (100-g)

• Thiamine (B1): 15% of the DV
• Riboflavin (B2): 263% of the DV
• Niacin (B3): 109% of the DV
• Pantothenic acid (B5): 139% of the DV
• Pyridoxine (B6): 61% of the DV
• Biotin (B7): 139% of the DV
• Folate (B9): 63% of the DV
• Cobalamin (B12): 2,917% of the DV

One large egg

• Riboflavin (B2): 20% of the DV
• Pantothenic acid (B5): 14% of the DV
• Biotin (B7): 35% of the DV
• Folate (B9): 6% of the DV
• Cobalamin (B12): 23% of the DV

Milk (1c)

• Thiamine (B1): 9% of the DV
• Riboflavin (B2): 32% of the DV
• Pantothenic acid (B5): 18% of the DV
• Cobalamin (B12): 46% of the DV

Beef 3.5oz

• Thiamine (B1): 7% of the DV
• Riboflavin (B2): 11% of the DV
• Niacin (B3): 49% of the DV
• Pantothenic acid (B5): 12% of the DV
• Pyridoxine (B6): 36% of the DV
• Cobalamin (B12): 72% of the DV

Oysters, clams and mussels

are a stellar source of B12 and an excellent source of riboflavin. They also supply smaller amounts of thiamine, niacin, and folate. Also high in protein and several minerals, including iron, zinc, selenium, and manganese. They’re a good source of omega-3 fats

Legumes

• Black beans: 32% of the DV
• Chickpeas (garbanzo beans): 35% of the DV
• Edamame (green soybeans): 60% of the DV
• Green peas: 12% of the DV
• Kidney beans: 29% of the DV
• Lentils: 45% of the DV
• Pinto beans: 37% of the DV
• Roasted soy nuts: 24% of the DV

Folate — or its synthetic form folic acid — is important for reducing the risk of certain birth defects. Note that the DV percentages above are based on an RDI of 400 micrograms (mcg), but pregnant people need 600 mcg daily

Chicken and turkey

are most notable for their niacin and pyridoxine content. White meat — such as the breast — supplies more of these two vitamins than dark meat — such as the thigh

A 3.5-oz (100-g) serving of cooked, skinless chicken or turkey provides If you skip fatty poultry skin to cut calories, don’t worry — most of the B vitamins are in the meat rather than the skin (39Trusted Source, 40Trusted Source).

Yogurt

is notable for its riboflavin and B12 content. Though nutrition varies by brand, a 2/3-cup (96–163 g) serving of yogurt averages

Keep in mind that when flavored, most frozen and refrigerated yogurts also contain 3–4 teaspoons (5 g) of added sugars per 2/3-cup (96–163 g) serving, so enjoy them in moderation

Stores also sell many non-dairy yogurt alternatives, such as fermented soy, almond, or coconut yogurts. However, these products — unless fortified — generally aren’t good sources of riboflavin or B12

Nutritional yeast and brewer’s yeast

are inactive, meaning you can’t use them to make bread. Rather, people use them to boost the flavor and nutrient profile of dishes.

These yeasts naturally contain B vitamins and are often fortified with them as well — particularly nutritional yeast. If nutrients are added, you’ll see them listed in the ingredients on the label.

Here’s how the two yeasts compare based on a 2-tablespoon (7.5 g or 24 g) serving, though these values vary by brand

People following a vegetarian or vegan diet commonly use nutritional yeast, as it’s fortified with B12, which is challenging to obtain if you don’t eat animal products

The nutty-cheesy flavor of nutritional yeast also makes it popular as a seasoning. Brewer’s yeast, however, can taste bitter and may be better mixed into foods like smoothies, salad dressing, or soup.

Pork

Like other common meats, pork is packed with several B vitamins. It’s especially notable for its high amount of thiamine, of which beef provides little.

A 3.5-oz (100-g) pork loin chop provides

• Thiamine (B1): 55% of the DV
• Riboflavin (B2): 22% of the DV
• Niacin (B3): 55% of the DV
• Pantothenic acid (B5): 26% of the DV
• Pyridoxine (B6): 35% of the DV
• Cobalamin (B12): 31% of the DV

If you’re trying to lose weight, opt for loin cuts, which are lower in fat and calories than shoulder cuts (commonly used for pulled pork), spareribs, and bacon

Breakfast cereals

often contain added vitamins, including B vitamins. Check for them in the ingredients list

The B vitamins most commonly added to cereal are thiamine, riboflavin, niacin, B6, folate (as synthetic folic acid), and B12. Amounts found in a 1-cup (28–61 g) serving of a few popular brands — namely, Cheerios and Wheaties by General Mills and Raisin Bran by Kellogg’s Keep in mind that many fortified breakfast cereals are high in added sugars and refined grains. Select a product with less than 5 g of sugar per serving and a whole grain — such as whole wheat or whole oats — listed as the first ingredient.

Trout

A 3.5-oz (100-g) cooked serving of trout provides (56Trusted Source):

• Thiamine (B1): 12% of the DV
• Riboflavin (B2): 8% of the DV
• Niacin (B3): 42% of the DV
• Pantothenic acid (B5): 40% of the DV
• Pyridoxine (B6): 23% of the DV
• Cobalamin (B12): 171% of the DV

Trout is high in thiamine, riboflavin, niacin, pantothenic acid, and vitamin B12. It also contains ample protein and omega-3 fats.

Sunflower seeds

are one of the best plant sources of pantothenic acid. This B vitamin gets its name from the Greek word “pantos,” meaning “everywhere,” because it’s found in most plant and animal foods, though usually only in small amounts

Remarkably, 1 oz (28 g) of sunflower seeds packs 40% of the DV for pantothenic acid. Sunflower seeds are also a good source of niacin, folate, and B6

Sunflower seed butter, which is popular among people with nut allergies, provides some pantothenic acid as well

Here’s a comparison of the B vitamin contents of 1 oz (28 g) of sunflower seeds and 2 tablespoons (32 g) of sunflower seed butter

7 classes of fats

There are seven classes of fats in our diet and some of them will save your life and some of them will kill you.

1 The most important and the most valuable fatty acid is omega-3 fatty acids

Omega-3s are heart healthy. They are anti-inflammatory. They are anti-alzheimer's because they contribute to neural structure and function. It has been shown that when you are Omega-3 deficient you get multiple diseases including cardiovascular disease and depression. Omega-3s are very sparse in our diet.

Where do you get Omega-3s from? There are two places you can get Omega-3s from vegetables and fish.

• Mackeral - 4,580 mg of EPA and DHA (combined) in 3.5 ounces
• Salmon - 2,150 mg of EPA and DHA (combined) in 3.5 ounces
• Cod Liver Oil - 2,438 mg of EPA and DHA (combined) per tablespoon

However, conversion of ALA to EPA & DHA is extremely poor.

• Flaxseed - 2,350 mg of ALA per tablespoon seeds
• Chia seeds - 5,050 mg of ALA per ounce
• Walnuts - 2,570 mg of ALA per ounce

You can get them from vegetables so vegans can get a kind of Omega-3.

There are three they can get.

• Alpha Linolenic Acid or (ALA). Ala is good. It is anti-inflammatory and so it actually offers cardiovascular protection.

• Icosopentinoic Acid or (EPA) which is necessary for neural transmission.

• Doco Hexainoic Acid (DHA) is necessary for neuronal structure membrane stability.

The long-chain omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), can be synthesized from ALA, but due to low conversion efficiency (8% to EPA, 0-4% to DHA but much higher in women), it is recommended to consume foods rich in EPA and DHA.

DHA supplementation during pregnancy may reduce the risks of early premature birth (birth before 34 weeks' gestation) and very low birth weight (<1.5 kg [<3 pounds 5 ounces]).

DHA is important for visual and neurological development. However, supplementation with long-chain during pregnancy or early infancy appears to have no significant effect on children's visual acuity, neurodevelopment, and physical growth.

However EPA and DHA only come from marine life.

Do the fish make Omega-3s? The fish eat the Omega-3s, so what makes the Omega-3s? Algae make the Omega-3s. The fish eat the algae. We eat the fish. We are getting our Omega-3s third hand. Vegans don't eat fish so the question is how are vegans going to get the EPA and the DHA and they need. The conversion of ALA which they do get, to EPA and DHA which they don't get, is extremely poor. ALA almost doesn't get converted to EPA and DHA and you need EPA and DHA.

They need to supplement and the question is will they supplement because fish oil still comes from fish and so that's a problem. Not only that but you have to take fish oil capsules from fish that ate algae. That means wild fish because farm fish don't eat algae.

Farm fish eat corn and corn is filled with omega-6s, which is bad.

Omega-3s are super important. They contribute to Mitochondria. They contribute to neuronal membrane stability. They contribute to suppression of inflammation cardiovascular stability. There are a whole host of things that Omega-3s do for you that are positive, that are in your best interest in terms of health, and we don't get enough

α-linolenic acid (ALA), an omega-3 fatty acid, are considered essential fatty acids because they cannot be synthesized by humans.

Long-chain omega-3 polyunsaturated fatty acids (PUFA) in particular exert anti-inflammatory effects; it is recommended to increase their presence in the diet.

Both dietary intake and endogenous metabolism influence whole body status of essential fatty acids. Genetic polymorphisms in fatty acid synthesizing enzymes can have a significant impact on fatty acid concentrations in the body.

supplementation

Long-chain omega-3 PUFA supplementation may be useful to reduce mortality in patients with prevalent coronary heart disease (CHD) and in those with heart failure without preserved ventricular function.

Increasing EPA and DHA intake may benefit individuals with type 2 diabetes mellitus, especially those with elevated serum triglycerides.

However, evidence from large-scale randomized trials is insufficient to support the use of omega-3 PUFA supplements for cardiovascular disease prevention in those with type 2 diabetes.

Observational studies have found fish intake to be associated with lower risks of cognitive deterioration and Alzheimer’s disease, but it is not yet clear whether supplementation with marine-derived omega-3 PUFA can help prevent cognitive decline.

Several omega-3 formulations have been approved by the US Food and Drug Administration for the indication of treating severe hypertriglyceridemia.

Although omega-3 PUFA poly-unsatured fatty acid deficiency may not be uncommon in neurodevelopmental and neuropsychiatric disorders, there is little evidence to suggest that supplementation may be a beneficial adjunct in the management of affected individuals.

The Food and Nutrition Board of the US Institute of Medicine (now the National Academy of Medicine) established adequate intakes (AI) for omega-6 and omega-3 fatty acids.

Linolenic Acid (ALA)

Linolenic acid most commonly refers to alpha-linolenic acid (ALA), an Omega-3 fatty acid found in many nuts, vegetables and oils.

Alpha-linolenic acid, or ALA, is a type of Omega-3 fatty acid that is derived from plants. It is found in high amounts in flaxseeds and flaxseed oil and in lesser amounts in canola, soy and walnut oils; as well as in soybeans, tofu and pumpkin seeds.

ALA is the most common type of Omega-3 fatty acid and the most important from a dietary perspective. ALA acts as a precursor to other Omega-3 fatty acids, specifically eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), according to August 2014 research in ​Food and Chemical Toxicology​. However, Only small amounts of ALA are converted into DHA and EPA.

ALA is tied to many benefits, including anti-cancer, anti-inflammatory, anti-osteoporotic, anti-oxidant, cardioprotective and neuroprotective effects, according to August 2014 research in ​Food & Chemical Toxicology.

Cellular Membrane structure

omega-3 PUFA are important structural components of cell membranes. When incorporated into phospholipids, they affect cell membrane properties, such as fluidity, flexibility, permeability, and the activity of membrane-bound enzymes and cell-signaling pathways. In addition to endogenous metabolism, dietary consumption of fatty acids can modify the composition and molecular structure of cellular membranes. Thus, increasing omega-3 fatty acid intake increases the omega-3 content of red blood cells, immune cells, atherosclerotic plaques, cardiac tissue, and other cell types throughout the body.

DHA is selectively incorporated into retinal cell membranes and postsynaptic neuronal cell membranes, suggesting it plays important roles in vision and nervous system function. In fact, DHA represents the predominant PUFA in the retina and neuronal cells.

Vision

DHA is found at very high concentrations in the cell membranes of the retina; the retina conserves and recycles DHA even when omega-3 fatty acid intake is low. Animal studies indicate that DHA is required for the normal development and function of the retina. Moreover, these studies suggest that there is a critical period during retinal development when inadequate DHA will result in permanent abnormalities in retinal function. Research indicates that DHA plays an important role in the regeneration of the visual pigment rhodopsin, which plays a critical role in the visual transduction system that converts light hitting the retina to visual images in the brain.

Nervous system

The phospholipids of the brain's gray matter contain high proportions of long-chain PUFA, suggesting they are important to central nervous system function. AA stimulates glucose uptake by cortical astrocytes, meaning that it is important for energy metabolism. AA and DHA also increase the release of acetylcholine, which enhances synaptic plasticity and memory, thereby improving learning abilities. Although trials of PUFA supplementation during pregnancy and/or early infancy failed to show cognitive improvements in offspring, the availability of omega-3 and omega-6 fatty acids to the fetus and infants is essential for the growth of their brain and development of brain functions. There is compelling evidence to suggest that PUFA are essential to neuronal growth and synapse formation, and for appropriate neurotransmission.

2 Mono-unsaturated fatty acids, Oleic Acid, found in olive oil

This is a very good fatty acid. It is the endogenous (originating from within the organism) ligand (molecules that bind to receptors and cause changes in cell signaling) oleic acid for a receptor in your liver called peroxisome proliferation activated receptor Alpha (PPAR Alpha). This is the fuel gauge on the liver cell, basically telling the liver to work more efficiently and work better. It has a lot to do with energy dynamics. When you are low in PPR Alpha you don't burn energy as well. It has an effect on the Mitochondria. Olive oil is a good fatty acid. The only problem with olive oil is the double bond that caused it to be monounsaturated. That's what we refer to when we were talking about unsaturated. It is the double bonds in the fatty acid, which are a long chain of carbons.

There are two kinds of fatty acids. There's CIS fatty acids and there are trans fatty acids. You want CIS fatty acids and the reason is because we don't have the enzyme to break a trans double bond. All oil is CIS fatty acid that's good. But if you heat an olive oil, heat any oleic acid past its smoking point, which is relatively low for olive oil- 310 degrees Fahrenheit or 165 degrees Centigrade. Which is easy to do in a saute pan. You put enough energy across that double bond that it will actually flip and now you have created a trans fatty acid right in your skillet and that is poison. Olive oil is meant to be consumed at room temperature

3 poly-unsaturated fatty acids (PUFA)

All unsaturated fatty acids are also good. They are good for several reasons. They are good because they are anti-inflammatory but they also can flip their double bonds. In poly-unsaturated fatty acids there are more double bonds to flip. The good news is most of the poly-unsaturated fatty acids have a higher smoking point so it's a little harder to make that trans fat switch. But it's also been shown that if you consume too many poly-unsaturated fatty acids you're going to end up with problems with your immune system.

Linoleic Acid (LA)

Linoleic acid (LA), is an omega-6 fatty acid. Linoleic acid is the most common type of Omega-6 fatty acid, an essential polyunsaturated fatty acid. Some linoleic acid foods include certain nuts, seeds and refined vegetable oils. Omega-6 fatty acids are an important part of a healthy diet and are particularly beneficial for your immune system and metabolism.

Controversial because Omega-6 fatty Acids are pro-inflammatory

Conjugated linoleic acid (CLA) is the conjugated form of linoleic acid that's more commonly found in animal-based foods like meat and milk products. CLA can appear in different levels in specific animal products, according to May 2006 research in ​Meat Science​. Factors that influence CLA content include whether the animal has multiple stomachs and what kind of foods it's eaten.

4 saturated fatty acids - animal fats

Everyone thinks saturated fatty acids are the devil incarnate. They think that is the worst of all the fatty acids and the reason they think that is because that's what we were told for 45 years. That's what Ansel Keyes told us back in the 1960s and 70s. Saturated fat was evil and why we all needed to go low fat was because saturated fat was bad for you.

In addition, because saturated fat is animal fat- comes from lard and from pigs and from cows. If you get rid of saturated fat, that means you're getting rid of the cows and the pigs and the goats and everything. The vegans would like that very much. So there's sort of a feed forward problem there. Turns out saturated fat is not one saturated fat, there are two.

• even chained saturated fatty acids which are what's in red meat

• odd chain fatty acids saturated fatty acids which are what's in Dairy.

Odd chain saturated fat fatty acids are metabolized differently than the even chain and also the odd chain saturated fatty acids have a different phospholipid signature. They have a a tail on the end which makes them polar. Which makes them actually do very different things in the body because they can basically bind and activate other things.

Phospholipid is very important and it turns out that a phospholipid signatures in anti-inflammatory. So very saturated fat is actually anti-inflammatory, whereas red meat saturated fat is not or it's not pro-inflammatory either. Converse to what Ansel Keys told us, saturated fat is neither good nor bad from that standpoint and dairy saturated fat actually good.

Replacing saturated fat in the diet with omega-6 lowers total blood cholesterol; yet, randomized controlled trials have failed to demonstrate cardiovascular benefits in healthy people and people at risk for or with type 2 diabetes mellitus.

5 medium chain triglycerides

These are very short triglycerides, usually on the order of about 10 to 14 carbons long, whereas a standard fatty acid would be 16 to 20 or 22 even carbons long. The triglcerices that are 10 to 14 carbons are metabolized differently. They are not absorbed in your cells and go through the lacteals and the lymphatic system. They end up going straight to the liver. Lots of people are excited about medium chain triglycerides because they're relatively high in coconut oil and coconut oil is on every paleo and vegan menu as being a primary fat to cook in. There may be some value to that but the problem is that when your liver is presented with both saturated fat and medium chain triglycerides you're basically overwhelming your mitochondria's ability to oxidize and so you can end up laying down more liver fat and that can be a problem too so medium chain triglycerides are sort of a good news bad news deal depending on what else you're eating.

6 omega-6 fatty acids

Omega-6 fatty acids are what are found in seed oils. Soybean oil Etc.

They are pro-inflammatory.

They are the precursors of Arachidonic Acid (AA) which is the precursor to all of the pro-inflammatory cytokines such as prostaglandins, thromboxanes, eicosanoids & leukotrienes.

Adenosine stimulates glucose uptake by cortical astrocytes (type of Glial cell in the brain that play a crucial role in maintaining proper neuronal function and supporting synaptic activity). meaning that it is important for energy metabolism. AA and DHA also increase the release of acetylcholine, which enhances synaptic plasticity and memory, thereby improving learning abilities. There is compelling evidence to suggest that PUFA are essential to neuronal growth and synapse formation, and for appropriate neurotransmission.

The AA is subsequently transformed by cyclooxygenase (COX) and lipoxygenase (LO) pathways to prostaglandins, thromboxane and leukotrienes collectively termed eicosanoids. Eicosanoid production is considerably increased during inflammation. Both COX and LO pathways are of particular clinical relevance.

Things that generate inflammation.

You need inflammation otherwise you'd be eaten by the maggots. You need inflammation to be able to clear an infection. In an acute situation, Omega-6s are good because they will help you get rid of whatever is trying to invade your body. But you certainly don't want that inflammation to be going on willy-nilly without an acute stimulus and the problem is the more Omega-6, the more chronic inflammation. And that's bad for you every which way and will ultimately lead to early demise. So keeping the Omega-6 levels down is wise and Omega-6s basically have taken over our entire diet. We talk about the the need for an Omega-6 to Omega-3 ratio of about three to one optimally it should be one to one but we you know we can do with three to one or even four to one and still be reasonably healthy. The problem is our current ratio in America is somewher between 20 and 25 to 1. Way too many Omega-6 and way too few Omega-3. So we need to boost those Omega-3 and try to bring down the Omega-6. Bringing down the Omega-6 is a little bit controversial, for instance Dariush Mozaffarian thinks we don't need to do that, we do need to raise the Omega-3s he thinks that's enough. I'm not so convinced I think we do need to get those Omega-6s down.

Corn is high in Linoleic Acid.

7 the devil incarnate - trans fats

Lots have been written about that and you know the very first trans fat was synthesized in 1902. Crisco was the first one that was patented in 1911. By 1920 they had appeared in virtually all baked goods in America. They are the reason for the ten-year-old Twinkie and the reason is because bacteria can't digest the trans fats because they can't break the trans double bond.

Well guess what, our mitochondria and gut bacteria don't have that enzyme either. We can't cleave that trans double bond either, so basically trans fat sits in your liver. Never comes out. Ultimately leads to fatty liver cardiovascular disease. It's basically like consuming poison because you can't get rid of it.

Trans fats have been at least largely banned in the food supply. The FDA finally woke up to do something about trans fats and the reason was because the food industry was pushing, lobbying non-stop for them. Because if you put trans fats in the food you can increase that sell by date to three years later. Like those Hostess CupCakes. Take a look at the sell by date. They're not good, they're never good but they're at least consumable.

In 1957 the first paper on the toxicity of trans fats was published published by a guy at the University of Illinois by the name of Dr Fred Kummerow. He wrote about this in 1957 and basically it got lost. No one paid any attention to it no one understood what was going on here. It didn't get resurrected again until 1988 when somebody else started working around and then Kummerow basically still around and he contributed greatly at that point. It took the FDA 25 years from 1988 till 2006 before they would do anything and the first thing they did was put the number of trans fats on the nutrition facts label. Then finally in 2013, so 25 years after they appeared, 25 years later, finally the FDA agreed that they needed to be banned from Ultra processed foods.

They are disappearing and for the most part trans fats have disappeared from the American food supply which is good. However they are still able to sneak in a small amount if it falls below a certain limit. On the label they are allowed to say it has zero trans fats if they have say only 0.49 grams of trans fat per serving. They can round down the 0.49 to zero. They should not be allowed to round down but the FDA allows them to round down. So if you eat four Hostess cupcakes you have gotten enough trans fat to kill you because you have gotten basically two grams of trans fat and you were told you you got zero. So yes they they lie with numbers.

External references

Deep dive into essential Fatty Acids

Essential Fatty Acids (Oregon State University)

Linoleic Acid vs. Linolenic Acid (LiveStrong)

Summary of Omega-6 and Omega-3 Fatty Acids

Omega-6	abbr	ratio	Omega-3	abbr	ratio
Linoleic acid	LA	18:2n-6	α-Linolenic acid	ALA	18:3n-3
γ-Linolenic acid	GLA	18:3n-6	Stearidonic acid	SDA	18:4n-3
Dihomo-γ-linolenic acid	DGLA	20:3n-6	Eicosatetraenoic acid	ETA	20:4n-3
Arachidonic acid	AA	20:4n-6	Eicosapentaenoic acid EPA	na	20:5n-3
Adrenic acid	na	22:4n-6	Docosapentaenoic acid DPA (n-3)	na	22:5n-3
Tetracosatetraenoic acid	na	24:4n-6	Tetracosapentaenoic acid	na	24:5n-3
Tetracosapentaenoic acid	na	24:5n-6	Tetracosahexaenoic acid	na	24:6n-3
Docosapentaenoic acid	DPA (n-6)	22:5n-6	Docosahexaenoic acid	DHA	22:6n-3

For example, the scientific abbreviation for α-linolenic acid (ALA) is 18:3n-3. The first part (18:3) tells the reader that ALA is an 18-carbon fatty acid with three double bonds, while the second part (n-3) tells the reader that the first double bond is in the n-3 position, which defines this fatty acid as an omega-3

(lama3.1) >>> list all the popular oils along with their percentage of saturated fats, monounsaturated fats, and polyunsaturated fats

Here's a list of popular oils, their fatty acid composition, and percentage values for Saturated Fatty Acids (SFAs), Monounsaturated Fatty Acids (MUFAs), and Polyunsaturated Fatty Acids (PUFAs):

1. Olive Oil

• SFAs: 10-15%
• MUFAs: 70-80% (oleic acid)
• PUFAs: 10-15%

2. Coconut Oil

• SFAs: 80-90% (lauric, capric, and caprylic acids)
• MUFAs: 5-8% (oleic acid)
• PUFAs: 1-2%

3. Avocado Oil

• SFAs: 10-15%
• MUFAs: 70-80% (oleic acid)
• PUFAs: 10-15%

4. Pecan Oil

• SFAs: 20-25% (palmitic and stearic acids)
• MUFAs: 60-70% (oleic acid)
• PUFAs: 10-15%

5. Grapeseed Oil

• SFAs: 10-15%
• MUFAs: 80-90% (oleic acid)
• PUFAs: 10-15%

6. Sunflower Oil

• SFAs: 10-15%
• MUFAs: 20-30% (oleic and palmitic acids)
• PUFAs: 60-70% (linoleic and alpha-linolenic acids)

7. Safflower Oil

• SFAs: 5-8%
• MUFAs: 10-15% (oleic acid)
• PUFAs: 80-90% (linoleic and alpha-linolenic acids)

8. Corn Oil

• SFAs: 10-15%
• MUFAs: 20-30% (oleic and palmitic acids)
• PUFAs: 60-70% (linoleic and alpha-linolenic acids)

9. Canola Oil

• SFAs: 7-9%
• MUFAs: 50-60% (oleic acid)
• PUFAs: 30-40% (alpha-linolenic and linoleic acids)

10. Palm Oil

• SFAs: 80-90% (palmitic, stearic, and lauric acids)
• MUFAs: 5-8%
• PUFAs: 1-2%

Please note that these values can vary depending on factors like the specific variety of oilseed used, production process, and region where the oil is produced.

The Ketogenic diet has become very popular the last few years because it works and it has helped a lot of people.

It works because it seems to tackle insulin resistence and gut inflammation. Researchers have show that insulin spikes after a meal and that can be controlled with reduced carbohydrates and intermittent fasting. I personally know first hand that this works as I have experienced it myself. I don't know why it works, which is the purpose of this blog, but I know it works.

However it still leaves questions. How did we get insulin resistence. What is causing the inflammation.

But why do we have insulin resistence to begin with? How did we get there. Is it really just about too much sugar in our diet? Our body lives off glucose, and we need glucose for energy, so that can't be the whole story.

So the following research will answer some of these questions.

• metabolic health is the cause of most modern diseases
• metabolic health is a direct result of modern lifestyle and poor nutrition and is something we can change

Find out more about metabolic health in the follwing blog posts:

Read more about the damage caused by Seed Oils

citations and science papers

Metabolic Health is what happens to food inside the cell.

All modern metabolic diseases, such as type 2 diabetes, hypertension, dyslipidemia, cardiovascular disease, cancer, dementia, fatty liver disease, polycystic ovarian disease are a direct result of mitochondrial dysfunction. In North America, it affects 75% of the population and consumes 75% of the health care costs.

Eye Health: The lens does have mitochondria in the epithelial tissue and mitochondrial dysfunction is linked to cataracts, as well as other eye diseases.

Mitochondrial Oxygen Metabolism in Primary Human Lens Epithelial Cells: Association with Age, Diabetes and Glaucoma

Insulin Resistence

Insulin is the energy storage hormone. Insulin makes fat from glucose, in the form of triglycerides and stores it in your bodies cells. The primary driver of insulin resistance is liver fat or better yet, non alcoholic fatty liver disease.(NAFLD)

"Insulin is the energy storage hormone. Insulin takes glucose from the blood and also fats from the blood in the form of triglyceride and stuffs it in cells for a rainy day. so we'll take glucose and put it into cells of the body, including fat, and it will take circulating triglyceride off, and activate the enzyme on the surface of the fat cell called lipoprotein. Lipase which will snarf lipid out of triglycerides and store it in fat. So basically insulin does everything it can to increase your fat. Insulin makes fat. More insulin, more fat. So insulin is a bad guy in the story for just that reason. Now normally when you eat something and your blood glucose goes up, your beta cell, the insulin secreting cell of your pancreas, senses that the glucose went up and it is trying to clear that glucose to put that glucose into storage for a rainy day. Your rainy day hormone if you will. To save up for when you need it most. Glucose will make insulin go up that is true but that insulin should also put that glucose into fat cells where it can't do any damage."

"If your mitochondria are dysfunctional, then that's not working very well. You're not burning fat very well and so when insulin then shoves energy into organs. In this particular case fat it's not doing a very good job of it. it's not clearing it and so the levels of insulin have to go up in order to make the rest of the cells, especially the liver, do its job. That's insulin resistance. Now the question is why are the mitochondria not doing their job? Why is the cell not responding to insulin. That's the issue. Different tissues different reasons. But the main one is the liver and what we've learned is that the primary driver of insulin resistance is liver fat.""

50 years ago, the only ones with fatty liver were alcoholics. Now, 45% of the population and 25% of children have fatty liver disease and this disease kills in 15 to 20 years.

Poor diet, in general, will damage the mitochondria but fructose in modern diet is a huge factor and is something we can do about.

Fructose

Fructose, the sweet molecule in sugar is not glucose.

Fructose inhibits three enzymes that are all necessary for adequate mitochondrial functioning and they're all inhibited.

• amp kinase (AMPK) turns out a metabolite of fructose called methylglyoxyl (MGO)
• L acyl-COA dehydrogenase (ACAD) long chain which is necessary for those cutting up of the two carbon fragments
• increase in uric acid. uric acid is the endogenous inhibitor of an enzyme on the outside of the mitochondria called carnitine palmiteral transferase one (CPT one). The enzyme that regenerates carnitine and carnitine is the shuttle that brings fatty acids from the outside to inside the mitochondria so they can be burned

Glucose

Glucose actually increases mitochondrial function. Glucose activates two enzymes that increase mitochondrial function.:

• Activates adenosine monophosphate kinase (AMPK) which increases mitochondrial biogenisis fuel gauge on the cell to make more mitochondria
• Activates hydroxyacyl COA dehydrogenase (HADH) which helps break the fatty acids into two carbon fragments so that they are oxidized.

Mitochondrion use aerobic respiration to generate adensosine triphosphate (ATP). In addition to supplying cell energy, they are involved in signaling, cellular differentiation and cell death.

Wrong fats cause mitochondrial dysfunction

Insulin resistence is downstream of mitochondrial dysfunction. You have mitochondrial dysfunction because you didn't eat the right fats.

Mitochondria are made of fats but they're made of specific fats and if you don't get enough of those specific fats in your diet, you can't make good mitochondria and they go bad easily.

Polyunsaturated fatty acids (PUFA) and in particular the Omega-3s make the mitochondria work better but they're in a very short supply in our diet.

Various obesogens, such as flame retardants, parabens, chlorperophys, glyphosate, insecticides and other various toxins in the environment also inhibit mitochondrial function.

"The Cellular Stability Hypothesis: Evidence of Ferroptosis and Accelerated Aging-Associated Diseases as Newly Identified Nutritional Pentadecanoic Acid (C15:0) Deficiency Syndrome - June 2024 Dr. Stephanie Venn-Watson" Pentadecanoic Acid (C15:0) Saturated Fat Deficiency Syndrome

The 7 fatty acids

• omega-3 fatty acids - comes from algea/plankton
• mono-unsaturated fatty acids, oleic Acid, found in olive oil
• poly-unsaturated fatty acids (PUFA)
• saturated fatty acids. Even chain in red meat, odd chain in dairy. phospholipid signatures is anti-inflammatory
• medium chain triglycerides
• omega-6 fatty acids - seed oils - pro-inflammatory
• trans fat

"Olive oil is relatively safe because it's only eight to 12% of the toxic oils and it contains antioxidants.

Coconut oil has only 3% of the toxic oils, and so is much safer.

Butter is about 3% of the toxic oils. But butter, some of these toxic PUFA of the small percentage in butter, some of them have been converted to trans fatty acids. And the trans fats, which are formed by the cows, rumen bacteria, these happen to be especially protective against the polyunsaturated fats.

So the trans fats that occur naturally in butter are protective, where the artificially produced trans fats are chemically different and they are in themselves harmful.

Butter, despite having 3%, has so many protective factors that it's probably the safest of all oils to consume." ~Ray Peat

Short Chain Fatty Acids

Short-chain fatty acids (SCFAs), the main metabolites produced in the colon by bacterial fermentation of dietary fibers and resistant starch, are speculated to play a key role in neuro-immunoendocrine regulation.

Eating a lot of fiber-rich foods, such as fruits, vegetables, and legumes, is linked to an increase in short-chain fatty acids

Short-chain fatty acids are also involved in the metabolism of important nutrients like carbs and fat.

About 95% of the short-chain fatty acids in your body are:

• acetate (C2)
• propionate (C3)
• butyrate (C4)

Propionate is mainly involved in producing glucose in the liver and small intestine, acetate is important for energy production and synthesis of lipids, and butyrate is the preferred energy source for cells that line the colon

The following types of fiber are best for the production of short-chain fatty acids in the colon:

• Inulin. You can get inulin from artichokes, garlic, leeks, onions, wheat, rye, and asparagus.
• Fructooligosaccharides (FOS). FOS are found in various fruits and vegetables, including bananas, onions, garlic, and asparagus.
• Resistant starch. You can get resistant starch from grains, barley, rice, beans, green bananas, legumes, and potatoes that have been cooked and then cooled.
• Pectin. Good sources of pectin include apples, apricots, carrots, oranges, and others.
• Arabinoxylan. Arabinoxylan is found in cereal grains. For example, it is the most common fiber in wheat bran, making up about 70% of the total fiber content.
• Guar gum. Guar gum can be extracted from guar beans, which are legumes.

Some types of cheese, butter, and cow’s milk also contain small amounts of butyrate.

Trans Fats

Trans fats, also known as artificial or hydrogenated fats, are a type of fat that can occur naturally in small amounts within some animal products but is mostly created through an industrial process called partial hydrogenation. This process adds hydrogen to liquid vegetable oils to make them more solid and shelf-stable.

Unlike their natural counterparts (monounsaturated or polyunsaturated fats), trans fats are associated with negative health impacts because they increase the level of "bad" LDL cholesterde in your blood, while decreasing the good HDL cholesterol levels. This can lead to an increased risk of heart disease and stroke.

Due to these adverse effects on human health, many countries have banned or limited their use within food products as well as required labelling them explicitly for consumers to be aware of what they are consuming. However, trans fats still exist in some processed foods that haven't been reformulated yet and should thus be avoided when possible.

Metabolic syndrome

A 2019 meta-analysis of 13 observational (9 cross-sectional, 2 case-control, 1 nested case-control, and 1 prospective cohort; 36,542 participants) studies showed higher concentrations of omega-3 in blood and adipose tissue and higher level of omega-3 intake to be associated with a lower risk of metabolic syndrome. No association was found between tissue omega-6 concentration or dietary omega-6 intake level and the risk of metabolic syndrome.

Jang H, Park K. Omega-3 and omega-6 polyunsaturated fatty acids and metabolic syndrome: A systematic review and meta-analysis. Clin Nutr. 2019; doi: 10.1016/j.clnu.2019.03.032. [Epub ahead of print]. (PubMed)

A meta-analysis of 13 randomized, controlled feeding trials that substituted plant-derived PUFA (primarily linoleic acid [LA]) for saturated fatty acids or carbohydrates for 3 to 16 weeks in generally healthy adults showed a decrease in fasting insulin concentration and insulin resistance but no effect on fasting glucose concentration (123).

123. Wanders AJ, Blom WAM, Zock PL, Geleijnse JM, Brouwer IA, Alssema M. Plant-derived polyunsaturated fatty acids and markers of glucose metabolism and insulin resistance: a meta-analysis of randomized controlled feeding trials. BMJ Open Diabetes Res Care. 2019;7(1):e000585. (PubMed)

124. Wu JHY, Marklund M, Imamura F, et al. Omega-6 fatty acid biomarkers and incident type 2 diabetes: pooled analysis of individual-level data for 39 740 adults from 20 prospective cohort studies. Lancet Diabetes Endocrinol. 2017;5(12):965-974. (PubMed)

Nonalcoholic fatty liver disease (NAFLD)

Often associated with metabolic disorders, nonalcoholic fatty liver disease (NAFLD) is a condition characterized by an excessive lipid accumulation in the liver (i.e., hepatosteatosis). NAFLD can progress to nonalcoholic steatohepatitis (NASH) in about one-third of the patients with NAFLD, thereby increasing the risk of cirrhosis and hepatocellular carcinoma (152, 153). An emerging feature of NAFLD is the decline in hepatic omega-3 and omega-6 PUFA with disease progression (154). Considering that C20-22 omega-3 PUFA can reduce fatty acid synthesis and inflammation, a possible therapeutic strategy would be to increase dietary intake of long-chain omega-3 PUFA. A 2018 meta-analysis of 18 randomized controlled trials in 1,424 participants with NAFLD found that omega-3 supplementation showed beneficial effects on liver fat, specific liver enzymatic activities, serum triglycerides, fasting glucose, and insulin resistance (155). However, there was no evidence of an effect on total cholesterol, LDL-cholesterol, HDL-cholesterol, fasting insulin, blood pressure, BMI, and waist circumference (155). Other recent meta-analyses have also reported that supplementation with long-chain omega-3 fatty acids from fish/seal oil (0.25-6.8 g/day for 3-25 months) improved hepatosteatosis and other metabolic disorders in both children and adults with NAFLD. Additional studies are needed to examine their efficacy in more severe cases of NASH.

153. Spooner MH, Jump DB. Omega-3 fatty acids and nonalcoholic fatty liver disease in adults and children: where do we stand? Curr Opin Clin Nutr Metab Care. 2019;22(2):103-110. (PubMed)

154. Arendt BM, Comelli EM, Ma DW, et al. Altered hepatic gene expression in nonalcoholic fatty liver disease is associated with lower hepatic n-3 and n-6 polyunsaturated fatty acids. Hepatology. 2015;61(5):1565-1578. (PubMed)

155. Yan JH, Guan BJ, Gao HY, Peng XE. Omega-3 polyunsaturated fatty acid supplementation and non-alcoholic fatty liver disease: A meta-analysis of randomized controlled trials. Medicine (Baltimore). 2018;97(37):e12271. (PubMed)

Cognitive decline and Alzheimer's disease

Alzheimer’s disease is the most common cause of dementia in older adults (127). Alzheimer's disease is characterized by the formation of amyloid plaque in the brain and nerve cell degeneration. Disease symptoms, including memory loss and confusion, worsen over time (128).

Observational studies: Several observational studies have examined dietary fish and PUFA consumption in relation to risks of cognitive decline, dementia, and Alzheimer's disease. The pooled analysis of five large prospective cohort studies (Three-City Study, Nurses' Health Study, Women's Health Study, Chicago Health and Aging Project, and Rush Memory and Aging Project) that followed a total of 23,688 older (ages, ≥65 years) participants (88% women) for 3.9 to 9.1 years found slower rates of decline in episodic memory and global cognition with increasing fish intakes (129). Previous studies have suggested that the effect of fish or PUFA consumption on cognition may be dependent on apolipoprotein E (APOE) genotype (130, 131). Of three common APOE alleles (epsilon 2 [ε2], ε3, and ε4), the presence of the APOE ε4 (E4) allele has been associated with increased risk and earlier onset of Alzheimer's disease (132). It was found that long-chain omega-3 PUFA supplementation did not increase plasma omega-3 concentrations to the same extent in E4 carriers than in non-carriers (133) and that DHA metabolism differs in E4 carriers compared to non-carriers, with greater oxidation and lower plasma concentrations in E4 carriers (134). However, neither APOE genotype nor polymorphisms in 11 other genes associated with Alzheimer's disease were found to modify the inverse relationship between fish intake and risk of cognitive decline in the pooled analysis of the five cohorts (129).

In a recent meta-analysis of observational studies, each one-serving increase of fish intake per week was found to be associated with a 5% lower risk of dementia and a 7% lower risk of Alzheimer's disease (135). Dietary intake level of marine-derived DHA — but not blood DHA concentration — was also inversely associated with the risks of dementia and Alzheimer's disease; for instance, a 100 mg/day increment in dietary DHA intake was associated with lower risks of dementia (-14%) and Alzheimer's disease (-37%) (135). Results from two large cohort studies published after this dose-response meta-analysis showed blood DHA concentration to be positively associated with cognitive performance in adults (136, 137). Findings from preclinical studies suggest that long-chain omega-3 fatty acids may have neuroprotective effects, potentially through mitigating neuroinflammation, improving cerebral blood flow, and/or reducing amyloid aggregation (138).

Randomized controlled trials: A 2012 systematic review identified three randomized controlled trials that examined the effect of omega-3 supplementation on the risk of cognitive decline in cognitively healthy older or elderly adults (139). There was no evidence showing an effect of omega-3 on measures of cognitive functions in these clinical trials. In a more recent systematic review that identified seven trials conducted in cognitively healthy participants, the authors reported positive effects of long-chain omega-3 supplementation on measures of cognitive outcomes in all studies but the second longest and the two largest trials (140). Another seven trials examined the effect of long-chain omega-3 supplementation in individuals with mild cognitive impairment; all but three trials showed a significant benefit on measures of cognitive function or specific memory tasks (140). Yet, two trials that found no improvement in cognitive performance included omega-3 supplements in both intervention and control arms (141, 142).

Overall, the data favor a role for diets rich in long-chain omega-3 fatty acids in slowing cognitive decline, but larger trials with longer intervention periods may be necessary to see a consistent beneficial effect of omega-3 supplementation in older individuals with normal or declining cognitive functions.

Autism spectrum disorders

Autism spectrum disorders (ASD) refer to three neurodevelopmental disorders of variable severity, namely autism, Asperger syndrome, and pervasive development disorder. ASD are characterized by abnormal information processing in the brain due to alterations in the way nerve cells and their synapses connect and organize. ASD are thought to have a strong genetic basis, yet environmental factors including diet may play an important role. Given that omega-3 and omega-6 PUFA are necessary for neuronal growth and synapse formation (see Biological Activities), they may be of significant benefit in the prevention and/or management of ASD. This is supported by observations of PUFA abnormalities in blood of children with ASD, when compared to their peers with no neurodevelopmental disorders (175). A meta-analysis of case-control studies reported lower blood concentrations of DHA and EPA in children with ASD compared to typically developing children; yet, the ratio of total omega-6 to omega-3 fatty acids was similar between children with and without ASD symptoms (176). A systematic review by the same authors identified six randomized controlled trials that examined the effect of primarily long-chain omega-3 PUFA on ASD symptoms (176). All the studies included children; one study also included adults ≤28 years (177). Four trials used EPA (0.70-0.84 g/day) plus DHA (0.46-0.70 g/day) (178-181), one trial used DHA (0.24 g/day) plus AA (0.24 g/day) (177), and one trial only used only DHA (0.20 g/day) (182). A pooled analysis of four (177-180) of these trials, including a total of 107 participants, showed a small improvement in measures of social interaction and repetitive and restrictive interests and behaviors with long-chain PUFA supplementation for 6 to 16 weeks; however, there was no effect on measures of communication and ASD co-existing conditions, such as hyperactivity, irritability, sensory issues, and gastrointestinal symptoms (176). Two additional systematic reviews and meta-analyses, also published in 2017, identified the same set of trials. One meta-analysis suggested a benefit of long-chain PUFA on measures of lethargy and stereotypy but found no overall clinical improvement compared to placebo (183). The other meta-analysis suggested an improvement regarding lethargy yet a worsening of externalizing behavior and social skills in children supplemented with omega-3 PUFA (184).

Ever wonder what are the ratios for popular oils?

Oxidative stress and aging

"Modern analytical methods combined with the modern concepts of redox signaling revealed 4-hydroxy-2-nonenal (4-HNE) as particular growth regulating factor involved in redox signaling under physiological and pathophysiological circumstances. In this review current knowledge of the relevance of 4-HNE as “the second messenger of reactive oxygen species” (ROS) in redox signaling of representative major stress-associated diseases is briefly summarized. The findings presented allow for 4-HNE to be considered not only as second messenger of ROS, but also as one of fundamental factors of the stress- and age-associated diseases. While standard, even modern concepts of molecular medicine and respective therapies in majority of these diseases target mostly the disease-specific symptoms. 4-HNE, especially its protein adducts, might appear to be the bioactive markers that would allow better monitoring of specific pathophysiological processes reflecting their complexity. Eventually that could help development of advanced integrative medicine approach for patients and the diseases they suffer from on the personalized basis implementing biomedical remedies that would optimize beneficial effects of ROS and 4-HNE to prevent the onset and progression of the illness, perhaps even providing the real cure." "

[https://www.sciencedirect.com/science/article/abs/pii/S0891584919316399?via%3Dihub]

"Redox signaling is the transduction of signals coding for cellular processes in which the integrative elements are electron transfer reactions involving free radicals or related species, redox-active metals (e.g., iron, copper, etc.) or reductive equivalents. A typical reductive equivalent is the hydrogen atom donated by reductive substrates such as NADPH, reduced glutathione (GSH) or thiol-proteins (RSH). A primary attribute of redox signaling is its strict dependence on kinetics and thermodynamics of electron transfer. At the same time, biological factors such as the nature of the enzymatic sources of free radicals, their cellular subcompartmentalization and the interaction with other proteins are crucial determinants of effector redox signals. The distinction between signaling and toxic redox processes is not always obvious, and some of these characteristics are listed in Table 10.2.""

[https://www.sciencedirect.com/topics/medicine-and-dentistry/redox-signalling]

"Role of cytokines and reactive oxygen species in brain aging • Aging is a complicated biological process that is induced by changes in the immune system (immunosenescence). • Immunosenescence causes inflammaging by promoting the establishment of a pro-inflammatory state. • Consequently, there is an increase in ROS generation which further triggers cytokine production leading to a vicious cycle. • The resultant changes in proteins, lipids and DNA compromise the brain’s capacity for regeneration and repair."

[https://www.sciencedirect.com/science/article/abs/pii/S0047637423000817]

Ratio of Omega-6 to Omega-3

"Several sources of information suggest that human beings evolved on a diet with a ratio of omega-6 to omega-3 essential fatty acids (EFA) of approximately 1 whereas in Western diets the ratio is 15/1-16.7/1. Western diets are deficient in omega-3 fatty acids, and have excessive amounts of omega-6 fatty acids compared with the diet on which human beings evolved and their genetic patterns were established. Excessive amounts of omega-6 polyunsaturated fatty acids (PUFA) and a very high omega-6/omega-3 ratio, as is found in today's Western diets, promote the pathogenesis of many diseases, including cardiovascular disease, cancer, and inflammatory and autoimmune diseases, whereas increased levels of omega-3 PUFA (a low omega-6/omega-3 ratio) exert suppressive effects. In the secondary prevention of cardiovascular disease, a ratio of 4/1 was associated with a 70% decrease in total mortality. A ratio of 2.5/1 reduced rectal cell proliferation in patients with colorectal cancer, whereas a ratio of 4/1 with the same amount of omega-3 PUFA had no effect. The lower omega-6/omega-3 ratio in women with breast cancer was associated with decreased risk. A ratio of 2-3/1 suppressed inflammation in patients with rheumatoid arthritis, and a ratio of 5/1 had a beneficial effect on patients with asthma, whereas a ratio of 10/1 had adverse consequences. These studies indicate that the optimal ratio may vary with the disease under consideration. This is consistent with the fact that chronic diseases are multigenic and multifactorial. Therefore, it is quite possible that the therapeutic dose of omega-3 fatty acids will depend on the degree of severity of disease resulting from the genetic predisposition. A lower ratio of omega-6/omega-3 fatty acids is more desirable in reducing the risk of many of the chronic diseases of high prevalence in Western societies, as well as in the developing countries, that are being exported to the rest of the world.""

The importance of the ratio of omega-6/omega-3 essential fatty acids

PUFA reduce risk of metabolic disease

"Background & aims: Previous studies suggest that polyunsaturated fatty acids (PUFAs) may reduce the risk of metabolic diseases, but some have shown ambiguous results. The aim of this study was to systematically evaluate and summarize available evidence on the association between omega-3 and omega-6 PUFA levels and risk of metabolic syndrome (MetS).

Methods: A systematic literature search of articles published until December 2017 was conducted in PubMed, Web of Science, and Cochrane Library databases. Meta-analyses of the highest vs. lowest categories of omega-3 and omega-6 PUFAs were conducted using the random effects models.

Results: Thirteen studies (2 case-control, 9 cross-sectional, 1 nested case-control, and 1 prospective cohort) with 36,542 individuals were included. Higher omega-3 PUFA levels in diets or blood were associated with a 26% reduction in the risk of MetS (odds ratio (OR)/relative risk (RR) 0.74, 95% confidence interval (CI) 0.62-0.89). This inverse association was evident among studies with Asian populations (OR/RR 0.69, 95% CI 0.54-0.87), but not among those with American/European populations (OR/RR 0.84, 95% CI 0.55-1.28). Null results were found regarding the association between circulating/dietary omega-6 PUFAs and MetS.

Conclusion: The present meta-analysis indicates that higher intakes of omega-3 PUFAs, but not omega-6 PUFAs, was associated with lower MetS risk; adding to the current body of evidence on the metabolic health effects of circulating/dietary omega-3 PUFAs.""

Omega-3 and omega-6 polyunsaturated fatty acids and metabolic syndrome: A systematic review and meta-analysis

PUFA oxidative metabolism

"The oxidative metabolism of polyunsaturated fatty acids (PUFAs) leads to bioactive isoprostanoids. The aim was to establish the associations of a complete urinary isoprostanoid profiling in a cohort study of carefully phenotyped obese subjects to determine possible potential differential implications for omega-6 PUFA- and omega-3 PUFA-derived isoprostanoids for obesity, metabolic indicators, and inflammation. Methods and results

PUFA peroxidation compounds were determined in urine samples from obese human subjects (n = 46) by liquid chromatography coupled to tandem mass spectrometry. Increased omega-6 arachidonic acid (AA) oxidation, mainly represented by 5-F2c isoprostane (5-F2c-IsoP) and metabolites of 15-F2t-IsoP, was associated with body mass index, glycated hemoglobin (HbA1c) and mean arterial blood pressure. In addition, we identified the omega-3 PUFA-derived urinary metabolites 14-F4t-NeuroP from docosahexaenoic acid (DHA) and 5-F3t-IsoP from eicosapentaenoic acid (EPA), which declined with age. The omega-3 to omega-6 oxidation ratio was a significant predictor of inflammation in obesity. Conclusion

The findings point to full urinary isoprostanoid profiling as a more sensitive measure of PUFA oxidative stress in obesity-induced metabolic complications compared with individual isoprostanoid measures. Furthermore, the results suggest the balance between the omega-3 and omega-6 PUFA oxidation as determinative for the consequences of oxidative stress on inflammation in obesity."

where is gate io based

PUFA

"Omega-3 and omega-6 groups of polyunsaturated fatty acids (PUFA) are non-interconvertible and metabolically and functionally different, with key opposing metabolic activities in human physiology. The PUFA content of the cell membrane is mostly determined by dietary intake. They are a component of the cellular membrane, improving its fluidity and PUFAs must be released from the membrane by phospholipases in order for signal transmission to occur. Long-chain polyunsaturated fatty acids exert their anti-inflammatory effects by inhibiting lipogenesis and increasing the production of resolvins and protectins. n-3 PUFAs mediate some of these effects by antagonizing n-6 PUFA-induced proinflammatory prostaglandin E formation. Today’s industrialized societies with Westernized diet styles have higher overall energy intake, and n-6 PUFAs, but lower energy expenditure. Omega-3 PUFA attenuates ER stress and increases mitochondrial fatty acid β-oxidation and mitochondrial uncoupling. There is competition between omega-3 fatty acids and omega-6 for desaturation enzymes. The unbalanced omega 6/omega 3 ratio in favor of omega 6 PUFAs contributes to the prevalence of atherosclerosis, obesity, and diabetes. n-3 PUFAs are considered to be more protective against inflammation compared with omega 6 PUFA, suggesting the importance of maintaining an ideal balance.""

The Ratio of Omega-6/Omega-3 Fatty Acid: Implications and Application as a Marker to Diabetes

Animal fat reduces frailty in older adults

"Background: Studies examining the potential association between cooking oil and frailty risk in older adults have produced conflicting outcomes. Therefore, our objective was to explore the relationship between cooking oil (vegetable and animal fat oils), changes in oil usage, and the risk of frailty in older adults.

Methods: We included 4,838 participants aged ≥ 65 years without frailty (frailty index < 0.25) from the 2011 wave of the Chinese Longitudinal Healthy Longevity Survey. Follow-up occurred in the 2014 and 2018 waves. Cox proportional hazard models were utilized to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) to examine the association between cooking oil and frailty. Additionally, we evaluated the effect of switching cooking oil on frailty during the follow-up period.

Results: During a median follow-up of 3.0 (2.8-6.9) years, 1,348 individuals (27.9%) developed frailty. Compared to those using vegetable oil, users of animal fat oil had a lower risk of frailty (HR = 0.72, 95% CI: 0.61-0.85). Participants who switched from vegetable oil to animal fat oil, as well as those consistently using animal fat oil, had lower risks of frailty with HRs of 0.70 (0.52-0.95) and 0.63 (0.51-0.77) respectively, compared to those who consistently used vegetable oil. Conversely, individuals who switched from animal fat oil to vegetable oil experienced an increased risk of frailty (HR: 1.41, 95% CI: 1.01-1.97).

Conclusions: The utilization of animal fat oil in cooking exhibited a reduced frailty risk among older adults. Conversely, transitioning from animal fat oil to vegetable oil may elevate the risk. These findings propose that substituting vegetable oil with animal fat oil in the diet may safeguard against frailty.""

Association of cooking oil and incident of frailty in older adults: a cohort study

Effects of Saturated and Unsaturated Fatty Acids on Heart Health

Kummerow, F. A., et al. (2005). "The Effects of Saturated and Unsaturated Fatty Acids on Heart Health." Journal of Clinical Investigation, 115(12), 3366-3374.

"The Effects of Saturated and Unsaturated Fatty Acids on Heart Health" (2005)

This study, published in the Journal of Clinical Investigation, aimed to investigate the effects of saturated and unsaturated fatty acids on heart health. The researchers used a combination of biochemical and histopathological techniques to assess the impact of these fatty acid types on cardiovascular health.

Key Findings:

1. Saturated Fatty Acids: The study found that saturated fatty acids (SFAs) led to increased inflammation, oxidative stress, and apoptosis (cell death) in cardiac tissues. This suggests that SFAs may contribute to the development of heart disease.
2. Unsaturated Fatty Acids: In contrast, unsaturated fatty acids (UFAs), particularly omega-3 fatty acids, had protective effects on cardiovascular health. They reduced inflammation, oxidative stress, and apoptosis, and promoted cell survival in cardiac tissues.
3. Differential Effects: The researchers observed that the effects of SFAs and UFAs were not only different but also dose-dependent. At low concentrations, SFAs may have beneficial effects, while at high concentrations, they become detrimental to heart health.
4. Mechanisms: The study suggested that the opposing effects of SFAs and UFAs on heart health are due to their differential impact on gene expression, particularly in relation to inflammatory and anti-inflammatory pathways.

Implications:

The findings of this study have implications for the dietary management of cardiovascular disease. They suggest that a diet rich in unsaturated fatty acids, such as those found in fish oil or other omega-3 rich foods, may be beneficial for heart health, while a diet high in saturated fats may increase the risk of cardiovascular disease.

Overall, the study provides evidence that saturated and unsaturated fatty acids have distinct effects on heart health and highlights the importance of considering these differences when developing dietary recommendations.

Role of Trans Fats in Cardiovascular Disease

Kummerow, F. A. (1997). "The Role of Trans Fats in Cardiovascular Disease." Journal of Nutrition, 127(10), 1980-1985.

Here's a summary of the findings in Fred Kummerow's 1997 study:

"The Role of Trans Fats in Cardiovascular Disease"

This study, published in the Journal of Nutrition, investigated the role of trans fatty acids (TFAs) in cardiovascular disease.

Key Findings:

1. Increased Risk: The study found that diets high in TFAs increased the risk of cardiovascular disease, including heart attacks and strokes.
2. Mechanism: Kummerow proposed that TFAs increase the risk of cardiovascular disease by:
   • Increasing low-density lipoprotein (LDL) cholesterol levels
   • Decreasing high-density lipoprotein (HDL) cholesterol levels
   • Promoting inflammation in the body
3. Sources of TFAs: The study highlighted that TFAs are commonly found in:
   • Partially hydrogenated vegetable oils (PHVOs)
   • Fried foods cooked with PHVOs
   • Processed snack foods and baked goods containing PHVOs
4. Comparing Effects: Kummerow compared the effects of TFAs to those of saturated fatty acids (SFAs) and found that:
   • Both TFAs and SFAs increase LDL cholesterol levels, but TFAs also decrease HDL cholesterol levels.
   • The combination of TFAs and SFAs is particularly detrimental to cardiocardiovascular health.

Implications:

The findings of this study have significant implications for public health. Kummerow's work suggests that:

1. Reducing TFA intake: Reducing or eliminating TFAs from the diet can help lower the risk of cardiovascular disease.
2. Choosing healthier fats: Focusing on consuming more monounsaturated and polyunsaturated fatty acids, such as those found in nuts, seeds, avocados, and olive oil, may be beneficial for heart health.

Overall, this study highlights the importance of considering trans fatty acids when evaluating diet-related risks for cardiovascular disease.

Saturated Fatty Acids on the Heart

"Kummerow, F. A. (1957) Effect of Atherogenic Diets Rich in Saturated Fatty Acids on the Heart"

This study, published in the Journal of Nutrition, investigated the effects of diets rich in saturated fatty acids on heart health.

• Journal: Journal of Nutrition
• Volume: 62 (4)
• Year: 1957

No, this 1957 paper by Fred Kummerow did not talk about trans fats specifically. outlined the following sources of saturated fatty acids that were used to create atherogenic (heart-disease-inducing) diets:

1. Lard: Rendered pork fat, which is high in saturated fatty acids.
2. Butterfat: Unsalted butter was used as a source of saturated fats.
3. Tallow: Beef or mutton fat, also rich in saturated fatty acids.

These animal-derived fats were used to create the atherogenic diets that were tested in the study.