Protein & Puberty

I study Alzheimer’s disease (AD) and there are a plethora of factors that go into your risk of developing the disease aside from genetics. It is not “type 3 diabetes” although insulin resistance is associated with AD and could also worsen the progression. There is also a protein in the pancreas that can clump together in a similar way as is seen in the brain in AD and cause pancreatic dysfunction, but the connection between these conditions is unknown. Type 3 diabetes actually refers to diabetes caused by this abnormal clumping as opposed to type 1 diabetes (innate lack of insulin) or type 2 diabetes (metabolically acquired lack of insulin). A good diet containing lots of vitamins, minerals, and anti-inflammatory compounds as well as exercise may reduce certain people’s risk of developing the disease and slow the progression of the disease somewhat. Specifically for Alzheimer’s you want to have a good amount of omega 3’s but not very much of other polyunsaturated fats. The reason for this is cellular lipid oxidation may be important for neuron death in AD and polyunsaturated fats are more easily oxidized than other fats. The majority should be monounsaturated fat but stay away from canola oil as that has been associated with negative outcomes in AD, olive oil is good instead. Saturated fat is good because it cannot be oxidized, and a lack of saturated fat will hurt brain and thyroid function, but too much will have adverse effects. Also for omega 3’s DHA and EPA are far superior to ALA. In terms of minerals magnesium, zinc, selenium, and manganese are the most important (magnesium does a ton of stuff but the other three support antioxidant enzymes, and zinc may have other benefits in AD). Fat soluble antioxidants such as vitamin E’s and A’s may help prevent lipid membrane oxidation and methoxylated flavonoids (flavonoids [plant antioxidants] with free hydroxyl groups are much more easily disposed of by the liver and kidneys and have trouble entering the brain, and usually have very little biological effect) may also prevent damage and prevent the toxic aggregation of amyloid beta peptides. There are a lot of other things that could theoretically be helpful, but they are more in the drug category rather than food and lifestyle. Remember that all of these things are theoretical and we still don’t know all of the causes or which ones are most important. There is some evidence that dietary intervention could slow the disease in some cases (slowed mortality but cognitive decline was not measured), but it is not known if it works as a preventative as well. This is a particularly weak study because it is really testing the effect of the diet on mortality and not the effect on AD related cognitive decline. It’s easy to look at correlations and say “This causes Alzheimer’s” but there are tons of non-genetic factors that correlate to AD, and different studies find varying levels of significance. The data in your video about fat and AD is looking at populations from all over the world, and you didn’t mention any studies that actually rigorously tested different fat intakes and the effect in AD. Genetics affects AD risk and the average genome of a Chinese person is very different from an average American. Not to mention all of the other differences in environment and diet and medicine not attributable to fat. The connection you draw between saturated fat and AD is purely speculation and there are many other reasons why the data could look the way it does. The biochemistry of AD is extremely complicated and a bad diet (associated with high saturated fat intake, but not caused by it) may play a role in disease risk or progression, but it is just a small piece of puzzle.