Mostly nutrition, this time around.
I’m working my way backwards through the archives at Conditioning Research. Here’s a trio of satisfyingly heterodox articles I found linked there:
CONCLUSION: A decline in serum total cholesterol levels may be associated with early stages in the development of dementia.
Although reported WG [Whole Grain] intake was significantly increased among intervention groups, and demonstrated good participant compliance, there were no significant differences in any markers of CVD risk between groups. A period of 4 months may be insufficient to change the lifelong disease trajectory associated with CVD. The lack of impact of increasing WG consumption on CVD risk markers implies that public health messages may need to be clarified to consider the source of WG and/or other diet and lifestyle factors linked to the benefits of whole-grain consumption seen in observational studies.
Somewhere in here I need to rant about the perils and pitfalls of observational studies. In this case: If you observe a bunch of people with low incidence of CVD, and note that they tend to eat a lot of whole grains, it does not follow that whole grains are heart-protective; it only follows that whole grans are correlated with a low-CVD-risk lifestyle in your sample population.
Consumption of processed meats, but not red meats, is associated with higher incidence of CHD and diabetes mellitus. These results highlight the need for better understanding of potential mechanisms of effects and for particular focus on processed meats for dietary and policy recommendations.
Speaking of heterodoxy, here’s a rather provocative piece of analysis from Dr. Stephanie Seneff on the link between low-fat diets, statins, and Alzheimer’s disease:
Note that while this is written in the style of an academic paper, as far as I can tell it is not itself peer-reviewed and published. It is however a synthesis of plenty of peer-reviewed and published work; you should probably rate it as at least a full step more trustworthy than this blog post. Here’s the abstract:
Alzheimer’s is a devastating disease whose incidence is clearly on the rise in America. Fortunately, a significant number of research dollars are currently being spent to try to understand what causes Alzheimer’s. ApoE-4, a particular allele of the apolipoprotein apoE, is a known risk factor. Since apoE plays a critical role in the transport of cholesterol and fats to the brain, it can be hypothesized that insufficient fat and cholesterol in the brain play a critical role in the disease process. In a remarkable recent study, it was found that Alzheimer’s patients have only 1/6 of the concentration of free fatty acids in the cerebrospinal fluid compared to individuals without Alzheimer’s. In parallel, it is becoming very clear that cholesterol is pervasive in the brain, and that it plays a critical role both in nerve transport in the synapse and in maintaining the health of the myelin sheath coating nerve fibers. An extremely high-fat (ketogenic) diet has been found to improve cognitive ability in Alzheimer’s patients. These and other observations described below lead me to conclude that both a low-fat diet and statin drug treatment increase susceptibility to Alzheimer’s.
(Nitpick: Ketogenic diets are very low-carb, not necessarily just high-fat. Ketosis — nota bene, ketosis is not ketoacidosis — is brought on by a lack of available glycogen.)
Now here’s Dr. Jaminet on that NYT “fat trap” piece:
- My theory of obesity, I: “The fat trap” (Perfect Health Diet)
I believe the brain defends not only (or primarily) an amount of fat mass, but also the health of the body, as reflected by the quantity and quality of lean tissue.
So it is plausible to speak in terms of set points, but there are two set points: a “fat mass set point”, and a “lean tissue quality set point.” The second is dominant: Lean tissue is essential to life, while gains in fat mass may diminish fitness in some environments but will increase fitness in others and are rarely catastrophic. So the tissue-quality set point usually dominates the fat mass set point in its influence upon the brain and behavior.
Definitely plausible, especially given some of the stuff I’ve dug up on the role of skeletal muscle in metabolism. But Dr. Jaminet loses points for proposing a mechanism that’s difficult to access:
Lean tissue is too important for health, and can be degraded in so many different ways, that signals about its state cannot be entrusted to a fragile, low-bandwidth mechanism like a hormone. Lean tissue signaling uses the high-bandwidth communications of the nervous system. This feedback system is hard for researchers to monitor.
We know damn well that hypertrophy in lean tissues is mediated by insulin, testosterone, growth hormone, and IGF-1 (among many others). Skeletal muscle hypertrophy — in response to exercise, for example — is accompanied by an increase in muscular insulin sensitivity, and protein intake in general tends to provoke a strong insulin response. Claiming that lean tissue metabolism is mediated by some sort of poorly-understood and hard-to-research nervous system feedback instead of the hormone activity listed above is extraordinary, and demands extraordinary evidence beyond “Well, most researchers only seem to care about total body mass because it’s easier to track”. As it stands, “nervous system feedback” comes across as an attempt to make the hypothesis as difficult to falsify as possible, which is the opposite of science.
Finally, to satisfy the “training” part of the title, here’s a pair of T-Nation articles on how to get wicked strong:
Picking a bar up off the ground and putting a bar overhead are both great ways to get strong. When combined into a single movement, they get even better.