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
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.
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)
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:
-
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.
-
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/
Glyphosate
Growing evidence that it is Glyphosate, the herbicide used in wheat crops, not actually gluten.
Cod liver oil is the best remedy for nearly all skin conditions—especially eczema. Cod liver oil contains three powerful nutrients:
-
Omega-3 fatty acids (DHA and EPA)
-
Vitamin A
-
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.
https://pubmed.ncbi.nlm.nih.gov/20427696/
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
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
contrary argument on vaers
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
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
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
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).
Pathologist Dr. Roger Hodkinson -they are lying about everything.
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
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/glyphosate-contamination-food-goes-far-beyond-oat-products
https://pubmed.ncbi.nlm.nih.gov/21294744/
-
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
-
Vitamin A - Difficulty seeing in the dark
-
Vitamin B1 - Nervous tension
-
Vitamin C - Swollen or red gums with slight bleeding
-
Vitamin D - Bone pain
-
Vitamin E - Muscle weakness
-
Vitamin K1 - Excessive bruising
-
Vitamin K2 - Tartar buildup
-
Calcium - Chronic cough
-
Iodine - Breast tenderness
-
Sodium - Overall weakness
-
Magnesium - Loss of energy
-
Potassium - Pounding in your ears when trying to sleep
-
Selenium - Brain fog
-
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)
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:
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.
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).
-
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)
-
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.
-
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)
-
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)
-
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.""
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."
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:
- 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.
- 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.
- 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.
- 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:
- Increased Risk: The study found that diets high in TFAs increased the risk of cardiovascular disease, including heart attacks and strokes.
- 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
- 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
- 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:
- Reducing TFA intake: Reducing or eliminating TFAs from the diet can help lower the risk of cardiovascular disease.
- 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:
- Lard: Rendered pork fat, which is high in saturated fatty acids.
- Butterfat: Unsalted butter was used as a source of saturated fats.
- 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.