Back comments section of the uric acid post _Flo passed on the news of the death, due to stomach cancer, of a prominent long term Optimal Diet follower. This is not the sort of in formation that should be ignored although, from an individual case, I doubt whether there is anything we will every actually find out about causation. The main thing it brings home forcefully is that none of us is immortal and a good diet will not allow us to automatically reach an advanced age. The OD and similar approaches brings marked improvement in many of the diseases of civilisation but clearly not all. For someone who has achieved remission from multiple sclerosis or ankylosing spondylitis it is depressing to accept that those same diet changes might not be cancer protective, or not completely so.
_Flo has made her own modifications to her diet which are sensible in their own right and represent her choices. As regards the type of cancer it quite interesting to note that Poland has one of the highest rates of stomach cancer in the world. This snippet was passed along by another friend on the net and is corroborated by pubmed. It does suggest that speculation based on the location/type of the tumour may not be representative a specific diet related factor, rather the result of living in Poland. Of course it might be diet related.
I have my own personal tweaks to the OD and do not see any clear way of improving what I have already achieved.
So let be set here in print. No one has all of the answers.
I thought I would take this chance to discuss the possibility that there are people for whom low carbohydrate eating might be genuinely problematic. I have picked up a couple of hints along these lines over the years, so here we go with some thoughts.
I discussed a secondary prevention trial for heart disease here. All of these people had glucose regulation problems (that's part of my definition of having a heart attack). Adding 500-600kcal of either corn or olive oil to a very low fat diet precipitated diabetes in two of these individuals. Why? That's a good question. Type two diabetes is intrinsically linked to insulin resistance. Normally people eating a bolus of fat will reduce the rest of their calorie intake to compensate. Anyone who didn't would have placed a significant carbohydrate load on top of fat induced insulin resistance (even vegetable oils induce this, although palmitic acid does a rather better job) and failed to deal with their relatively high carbohydrate intake. Pure speculation but a low fat diet, with 80ml of added vegetable oil, undoubtedly triggered 2 cases of type two diabetes. I found that interesting.
Second hint was Jenny Ruhl's comment that she had come across very, very occasional individuals with diabetes who responded to low carbohydrate eating by deterioration of glycaemic control. Again, I have no details what so ever but anyone's ears should prick up when they hear things like this. Denial is not where it's at.
Then Carb Sane introduced me to the Otsuka Long-Evans Tokushima Fatty strain (OLETF) of rats. These rats are a diabetologists dream. Under fixed isocaloric conditions they gain weight and fat mass in direct proportion to the percentage of fat in an exactly measured 28.7 joule daily ration. Like, wow. Fat really does make you fat!
Of course the OLETF rat is described as a Good Model for human type two diabetes. It explains exactly why all diabetics put on to a LC, high fat diet become obese and hyperglycaemiac. What do you mean, they don't? Oh, not enough testosterone! The OLETF rats only become diabetic if they are male. That's why all type two diabetics are blokes. What do you mean, women get type two diabetes? But out model says only blokes should. And it's a Good Model...
OK facetiousness aside, what is happening in the OLETF rats? Is it possible that there are some humans out there with OLEFT rat style type two diabetes. Well, why not?
Let's have a look at what is happening from the point of view that insulin is the primary hormone in the development of obesity. If you think about someone eating just once a day, essentially all of their calories are going to get stored. Glycogen in the liver and fat in the fat. What determines weight gain is how much of that stored energy fails to be extracted from storage before the next meal arrives.
Summary: No one stores lipids or glucose in their blood stream. It all goes in to short term storage. What comes out determines weight loss. Insulin determines what comes out.
OLETF rats, on high fat, fixed calorie diet of 28.7 joules per day put all of this energy in to storage but fail to extract as many of these calories/joules from storage as those OLETF rats on 28.7 joules of a high starch diet. What is going on?
If you accept the insulin hypothesis of weight gain, the answer is that dietary fat is being trapped in adipocytes by excessive blood insulin. There must be excess insulin.
Why is the insulin elevated when there is a reduced dietary stimulus for insulin production? These rats have peripheral, almost certainly muscle based, insulin resistance. But only on a high fat diet.
High fat diets put lipids in to muscles, muscles full of lipid don't accept glucose. If the system works correctly the muscles run on lipids until there is a balance between fat supply rejecting glucose and fat depletion allowing glucose acceptance. A few billion years is ample time to get this system working correctly to maintain normoglycaemia in the face of varied macronutrient intakes from day to day.
What might be broken in this system in the OLETF rat?
Well, if you can get lipids in to muscle cells but cannot then use that lipid for beta oxidation you would expect to develop muscle insulin resistance in proportion to the amount of fat you supply, ie if the fat enters the muscles but does not go any further those muscles will become insulin resistant and stay insulin resistant. If muscles are not accepting glucose because they are insulin resistant the glucose is going to have to be dealt with by increased levels of insulin. Hyperglycaemia is unacceptable.
The extra insulin needed to maintain normoglycaemia then traps stored dietary fat in adipocytes. The rats get fat because they cannot get fat out of adipocytes. They will also do less running around and will probably feel colder than normal rats because they have no access to their fatty tissue for energy supplies. If they had access to food they would eat more, but 28.7 joules per day was the limit in this experiment. If they had access to more calories they would clearly eat more because no one likes the hunger and shivering produced by sequestering a chunk of your caloric fat intake in your adipocytes and locking it in there with insulin.
Once your fat cells get full enough they will spill free fatty acids because they are now too full to listen to insulin any more. These FFAs join those intra cellular muscle tissue di and tri glycerides from the metabolic defect. Intra myocyte fatty acids still have no where to go, so muscle insulin resistance rockets, plasma glucose rockets and you have a superb model of fat induced obesity and peripheral insulin resistance.
Glucose enters mitochondria as pyruvate. Fatty acids enter mitochondria as acyl CoA moieties. The place to be looking for explanations for the syndrome seen in the OLETF rat is in fatty acid processing. My guess is that lipid molecules get in to myocytes but never get effectively passed to the mitochondria. Quite what testosterone has to do with this is beyond me, it's not me that is suggesting the OLETF rat is a good model for human type 2 diabetes!
You have to ask what would have happened on a ketogenic diet. Would ketosis have side stepped this problem? Ketone bodies enter mitochondria without any need for long chain fatty acid transporters. They use monocarboxylate transporters, just like pyruvate... You don't really think that Kaneko et al would so something as stupid as putting an OLETF rat on a ketogenic diet? But it would have been interesting. I'm not sure it would side step the problem but it might. I'm certainly not expecting a diabetologist to find out for me.
I really enjoyed the OLETF rat. Does it tell me something about type two diabetes? Only that there might be very, very special people who respond to dietary fat with hyperglycaemia.
I never did find any teeth in my chickens. I understand hen's teeth are rare. So are OLETF humans.
But they probably exist (not the hen's teeth!).