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David Brown's avatar

Does anyone find it odd that no obesity expert anywhere in the World can plausibly explain what caused the global obesity/diabetes epidemic? In my view, the most likely explanation has to do with changes in animal husbandry. Excerpt from Page 56 of 'Omega Balance' by Australian zoologist Anthony Hulbert, PhD (2023) "The contribution of “pork and poultry” to animal-sourced foods was 20 percent in 1961 and 41 percent in 2018…Between 1961 and 2018 there was a dramatic worldwide increase in the supply of fats from sources that have very low omega balances. Fat from “pork and poultry” was greatest in North America for the entire 1961-2018 period, while for Australia and South America, the contribution from “pork and poultry” was the World average level in 1961 and showed the greatest absolute increases (about 16 g) over this period to be similar to North America and Europe in 2018. There was negligible change in Africa over this period."

Here's a clue as to what made the food supply obesogenic. "It is true that the vast advancement in technological developments has led to a reduction in physical activity worldwide, but as obesity now involves infants and the populations of developing countries, this obesity pandemic cannot be attributed to this alone. In addition, laboratory and other domesticated animals have also been subject to the increased prevalence of obesity, despite having largely unchanged living conditions for many years." https://www.intechopen.com/chapters/41405

Steve Blechman explains why the Mediterranean style dietary approach consistently produces favorable results. "The Mediterranean diet is low in arachidonic acid and rich in healthy fats such as monounsaturated fats found in extra-virgin olive oil (EVOO), nuts and omega-3 fatty acids from fish, which has been shown to lower the risk of inflammation, heart disease, cancer, diabetes and obesity, and other degenerative diseases." dvancedmolecularlabs.com/blogs/news/new-red-meat-study-controversy

Another clue as to where the problem lies. "Endocannabinoids and their G-protein coupled receptors (GPCR) are a current research focus in the area of obesity due to the system's role in food intake and glucose and lipid metabolism. Importantly, overweight and obese individuals often have higher circulating levels of the arachidonic acid-derived endocannabinoids anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) and an altered pattern of receptor expression. Consequently, this leads to an increase in orexigenic stimuli, changes in fatty acid synthesis, insulin sensitivity, and glucose utilisation, with preferential energy storage in adipose tissue." https://pmc.ncbi.nlm.nih.gov/articles/PMC3677644/

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Joan Breibart's avatar

YOU must be very young in age.EVERYONE who is above age 60 KNOWS that obesity is a direct result of quitting SMOKING and taking cup "health." It has nothing to do with WHAT we eat or drink. ONLY HOW MUCH and how often. MONEY!!! Few people ate in restaurants and no everyone does-- even people on welfare. The portions are huge since we know that it costs only $2.00 to make a plate of noodles ( PASTA). So to charge $18.00 = a huge number of BITES. Playing with food is what wellness is all about; it will go bye bye as the GLP-1 drugs are soon in all of our bodies whether for fatness or addiction or even serious illness.

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David Brown's avatar

I'm 77. I've been perusing nutrition information and experimenting with my nutrient intake for 48 years. Metabolically, I'm healthy. Physiologically, I'm a train wreck because of excessive linoleic acid intake (peanut butter, mayonnaise, soybean oil) and excessive arachidonic acid intake (99% fat-free turkey meat).

It is interesting that free range cheetahs are healthy and captive cheetahs diseased due to differences in polyunsaturated fatty acid intake. Differences in exercise levels, and (in the case of captive cheetahs) lack of periodic fasting exacerbate the damage that results from excessive polyunsaturated fatty acid intake. Excerpt: "The high proportion of antelope in the free-ranging cheetah diet is expected to result in a lower proportional intake of unsaturated fat, since the unsaturated to saturated fat ratio in ruminant tissues is substantially lower than in monogastric animals. Ruminant muscle tissue typically has an unsaturated to saturated FA ratio of between 0.11 and 0.15, while the ratio in donkey meat is around 1.45. The specific components and organs of prey animals consumed by free-ranging cheetahs should also lead to lower serum PUFA to SFA ratios, as the intra-abdominal fat depots, frequently consumed by free-ranging cheetahs, also have a higher proportion of saturated fat than either intramuscular or subcutaneous adipose tissue. Most African ungulates have substantial intra-abdominal fat reserves, including, mesenteric, omental, perirenal and channel fat. Consumption of whole prey carcasses is therefore likely to result in an increased intake of dietary fat compared to captive diets that are mostly limited to muscle meat and bone."

Impact of exercise and fasting: "The increased proportional intake of dietary fat, decrease in feeding frequency and increased physical activity in free-ranging compared to captive cheetahs are all predicted to result in enhanced mitochondrial FA oxidation through the lowering of circulating glucose concentrations and insulin:glucagon ratios. During fasting/refeeding cycles and increased levels of exercise, tissue PUFA concentrations have been shown to deplete rapidly in both humans and rats. These studies show that most PUFAs, including α-linolenic acid (ALA) and linoleic acid (LA), are preferentially oxidized in periods of exercise or fasting. During refeeding, SFAs and monounsaturated fatty acids (MUFAs), such as palmitic acid and oleic acid, are also more rapidly replaced than any of the PUFAs. Similarly, the concentrations of most plasma PUFAs and MUFAs have been shown to be significantly lower in rats fed a high fat ketogenic diet than in controls. The predicted increase in FA oxidation in free-ranging cheetahs is therefore likely to also skew their serum FA profiles toward lower proportional serum concentrations of PUFAs and MUFAs relative to SFA." https://pmc.ncbi.nlm.nih.gov/articles/PMC5167222/

The point is, both exercise and periodic fasting furnish protection from the impact of excessive polyunsaturated fatty acid intake. Note that "Fatty acid composition in the Western diet has shifted from saturated to polyunsaturated fatty acids (PUFAs), and specifically to linoleic acid (LA, 18:2), which has gradually increased in the diet over the past 50 y to become the most abundant dietary fatty acid in human adipose tissue." https://pmc.ncbi.nlm.nih.gov/articles/PMC9060469/

Immunity-wise, excessive polyunsaturated fatty acids stored in adipose tissue increases risk for COVID-19 complications. "Separately, on analyzing global COVID-19 mortality data and comparing it with 12 risk factors for mortality, they found unsaturated fat intake to be associated with increased mortality. This was based on the dietary fat patterns of 61 countries in the United Nations' Food and Agricultural Organization database. Surprisingly, they found saturated fats to be protective." https://www.medpagetoday.com/reading-room/aga/lower-gi/86940

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Joan Breibart's avatar

get a life.

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David Brown's avatar

Thanks for the advice but I already have a life. https://johnditragliamd.substack.com/p/the-other-fat-science

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