Wild-Caught Salmon and Metabolic Health

Related to the high-fat vs low-fat debate, there is an interesting article to shake up our thinking: Study of Alaska Natives confirms salmon-rich diet prevents diabetes, heart disease. It states that, “A diet of Alaska salmon rich in Omega-3 fatty acids appears to protect Yup’ik people from diabetes and heart disease — even when the individuals in question have become obese, according to a recent study that examined eating habits and health in the Yukon Kuskokwim Delta region. […] Something was different, and it didn’t appear to be genetics. […] “Interestingly, we found that obese persons with high blood levels of Omega-3 fats had triglyceride and CRP concentrations that did not differ from those of normal-weight persons,” Makhoul concluded.” Now that is fascinating. There could be a lot going on with this population, but they do make for a useful comparison.

To begin, it should be noted that these Inuit/Eskimos are on average overweight, similar to other Americans. Yet they have some of the lowest rates in the world of metabolic syndrome and obesity-related diseases like diabetes. This is in spite of their no longer being entirely on a traditional diet. They are getting plenty of crappy processed and packaged foods, in line with the industrialized Standard American Diet (refined grains, high fructose corn syrup, seed oils, etc). And these native Alaskans are unhealthy in other ways, as obesity isn’t a good thing. But those large doses of healthy unoxidized Omega-3s from wild whole foods seem to be their saving grace. It is true that most Americans are getting too many inflammatory Omega-6s and increasing Omega-3s is already known to decrease inflammation. That is all the more reason to eat fresh cold water fish, assuming it’s wild-caught in clean waters (it’s too bad we’re overfishing the oceans). Or, failing that, supplements might be beneficial; including algae-based sources.

That might go against the argument of those like Dr. Paul Saladino who speculate all polyunsaturated fats (PUFAs) are problematic at high intake; whether Omega-6s or Omega-3s, industrial or whole, oxidized or fresh; and no matter the PUFA ratio. The argument is all PUFAs will oxidize, even in the body after consumption because the unsaturated carbon bonds are unstable in being able to pick up oxygen atoms and the body can only handle so much oxidization using its limited supply of self-produced antioxidants and dietary antioxidants. The system overwhelmed by oxidized PUFAs is unable to contain the free radicals that wreak havoc with oxidative stress. But is that excess PUFA theory true? The jury is still out on that. Even if too many PUFAs overall might still be harmful in other ways, the recent Inuit study indicates certain PUFAs maybe can’t be blamed for metabolic syndrome and such.

It would be useful to look at these Inuits’ total PUFA intake and Omega-6 to Omega-3 ratio, which determines inflammation levels. And one might wonder about a causal link between inflammation and insulin resistance. Of course, as Dr. Saladino would argue, it might be simpler to just remove all the processed carbs and industrial seed oils; rather than try to counteract the harm with more Omega-3s. But if your (carb-caused, stress-induced, etc) cravings or other factors beyond your control have compelled you to eat a health-destroying diet that has made you fat or otherwise metabolically unfit, not to mention inflamed and maybe with high LDL (a response to inflammation), then by all means glug down some Omega-3s as medicine. It is known to have numerous health benefits, at least for those on an unhealthy diet, including this other evidence for possibly preventing/reversing insulin resistance and diabetes. You might slowly die of some other dietary-related disease, but at least you’ll lessen a large swath of health problems and feel relatively better.

Dietary details and confounders aside, this study blows the anti-fat crowd out of the water, including those like Ted Naiman who argue for low-carb, high-protein, and moderate fat. This seriously challenges the claim that the carbohydrate-insulin hypothesis is dead and that it’s simply about energy excess, either carbs or fat (or both). Ben Bikman, a leading insulin expert and active researcher, still thinks the carbohydrate-insulin hypothesis is valid and his view appears to be supported or not contradicted, according to this data. But, if nothing else, this new evidence clearly keeps the debate undeniably alive and even more compelling, however it might remain unresolved in continuing disagreements. What is refuted is the sweeping declaration that all energy excess, though surely sometimes a valid factor, can apply to every form of dietary energy under all conditions and in all diets.

It really does matter what kind of fat one is eating. Then again, it also matters what kind of carbs (Dr. Saladino thinks honey might be metabolically different, a whole other contentious debate). Talking about macronutrients as general abstract categories may not always be helpful. Sure, many people can lose fat by restricting calories or particular macronutrients. Both low-carb, high-fat diets and low-fat, high-carb diets can cause some people to naturally reduce calorie intake because there is nothing that causes overconsumption like the fattening powerhouse of carb-fat combo. And no doubt one could choose to increase protein, instead. But even if one eats high-carb, high-fat diet and so unsurprisingly becomes obese, it doesn’t follow that metabolic syndrome is inevitable. In that case, the healthy fats might protect one against metabolic syndrome, even on an industrial diet. If this is confirmed, Omega-3s not only balance excess Omega-6s but also excess simple carbs.

This seems to imply the unoxidized Omega-3s from fresh wild-caught whole foods is maintaining insulin sensitivity, despite the fact that all those carbs typically would be causing insulin resistance. That is the really interesting part. The whole point of the carbohydrate-insulin hypothesis is that excess glucose in the blood eventually overtaxes the body’s capacity and throws off the hormonal system, specifically the hormone insulin but also possibly involving insulin-glucagon ratio. The hormonal system acts as locus of messaging and control for multiple other systems, including metabolism. With insulin resistance, fat simply gets stuck in fat cells and can’t be accessed. So, the individual gets hungry and eats more. Interestingly, long-term fasting can sometimes kick insulin sensitivity back in gear and so the body will start burning the fat. That mechanism described is what the carbohydrate-insulin hypothesis is all about. That is the theory that supposedly down for the count.

Maybe we need another theory. As countering the harm described by the carbohydrate-insulin hypothesis, we could call it the fat-insulin hypothesis or, to be more specific, the Omega3s-insulin hypothesis. This might relate to how certain fats promote fat-burning, specifically in terms of Stearic fat (in tallow) which is a saturated fat, the supposedly worst fat. It apparently means eating energy as this kind of fat not only increases metabolism but encourages the release of the bodies energy stored as fat. This presumably would have to include a role of insulin sensitivity, the opposite of insulin resistance. It’s true that eating lots of Stearic acid on a high-carb industrial diet while obese and metabolically unfit might not be all that helpful. As another factor, consider that wild-caught fish would be higher in fat-soluble vitamins and micronutrients. The fat-soluble vitamins play a powerful role similar to hormones. In that case, it might be a fat-soluble-vitamin-insulin hypothesis, but that is getting a bit wordy. Context, as always, is king. Obviously, we need to get away from overly simplistic generalizations. The macronutrient model is as unhelpful as the caloric model, if not combined with more detailed knowledge.