COMMENT: A larger pancreas is not necessarily "bad," and in any case can be explained by simpler factors than postulating overcompensations due to cooking. A difference between humans and another species may be explained by any of the major factors that differ between the species. That is, the difference in pancreas size between species is not necessarily due to diet (though it might be, depending on specific circumstances); this follows from the principles discussed in Pagel and Harvey [1988].

As for the comparison between different human populations, a larger pancreas and larger salivary glands may result from many other factors than the supposed necessity of producing more enzymes due to cooking. In particular, a simpler and more reasonable suggestion would be that eating more carbohydrates (whether heat-treated or not) increases the secretion of insulin, subject to investigation of course. (Generally, people eating heat-treated carbohydrates would be likely eat to more carbohydrates, of course, since such carbohydrates are denser in calories, and cooked starch foods are usually softer and easier to eat than raw starch foods.)

Concerning enlarged salivary glands, the first point to note is that Howell never provided any hard proof that having larger salivary glands is necessarily a pathological condition. We will see below that while certain health disorders are associated with larger salivary glands, that does not necessarily imply the converse is necessarily true, i.e.:

specific health disorder = (implies) enlarged salivary glands

enlarged salivary glands = health disorder or bad health.

Controlled data on size of salivary glands is mixed. In relation to salivary glands specifically, this brings us to the the second point for discussion here, which is that the evidence relating their size to diets is mixed. Etzel [1993, p. 136] cites two studies that show diets high in tannins can increase the size of the salivary glands. Cooking can deactivate some tannins, while increasing the bioavailability of others by concentrating them in cooking broth/water.

Etzel [1993, p. 140] reports that protein deficiency can reduce the size of salivary glands in test animals. He also cites studies (pp. 137-138) showing mixed results of diets that are calorie-restricted: some diets showed decreases, others increases in salivary gland sizes.

What can be concluded? Putting the above information together, since conservative cooking increases the bioavailability of protein and energy (e.g., digestion of cooked starch is more efficient than raw), the hypothesis that a cooked diet might produce larger salivary glands than a similar raw diet seems plausible. That is, the effect of cooking (if any) on the size of the salivary glands may actually be the effect of increases in the bioavailability of protein, and/or increased absorption of tannins (rather than the lack of enzymes). So what, if any, conclusions can be drawn, then?

Although the salivary glands can enlarge due to certain specific health disorders--e.g., sialadenosis; see Rossie [1993]--Howell produces no evidence that the general kind of enlargement he discusses is pathological or harmful in any way. And finally, the most important point here is that there is no credible evidence that links the change in size of salivary glands to the lack of enzymes in cooked foods.

Since cooked starches are actually more easily digested than raw, enzyme production is not the real issue here. Finally, the question of starch digestion is probably of minor importance here, in any event. In general, cooked starches are easier to digest than raw starch foods; see Kataria and Chauhan [1988], Bornet et al. [1989] for some specific examples. Note that cooked starch is extremely easy to digest (humans and cattle are easily "fattened" with cooked starch), and if one replaces starch by other foods, there would be a need to produce other enzymes anyway. Thus, despite the fact that cooking destroys enzymes in raw starch foods, the end result (cooked starch) is easier to digest than raw starch. Consequently, if Howell's claim that populations eating more heat-treated carbohydrates have a larger pancreas and salivary glands is true, then as mentioned previously, the simplest hypothesis is that it is explained by the larger volume of carbohydrates eaten, since fewer enzymes per unit of volume would be required.

COMMENT: The above claims are made in Howell [1985], but the evidence provided for them is, quite frankly, sloppy and logically invalid. The evidence for the claims regarding brain size is presented in Tables 5.1-5.3, pp. 75, 77 of Howell [1985]. However, a look at the tables reveals that in every case, Howell is mixing data from different researchers, as well as the critical point that renders his comparison invalid: he is comparing data from what appear to be different species and/or strains of rat. That is, a difference in brain size between different species (or strains) is not necessarily due to differences in diet (this is a generalization of Pagel and Harvey [1988]). And of course, Howell's claim that the size difference is due to enzymes in the diet is nothing but speculation on his part, in any event.

Howell's data on pancreas size is similarly sloppy and logically invalid. Howell says [1985, p. 82]:

...[F]eeding one group of mice a raw diet, and another group the same food cooked (and therefore enzymeless). A reasonable period to complete the job would be two months. The animals would then be dissected and each pancreas weighed. But all you would have to do is read about this laborious experiment; the work has already been done.

The data cited by Howell do not meet the above stipulated experimental requirements. The data in support of the claims of pancreas size differences is given in Tables 5.7-5.9 of Howell [1985, pp. 81, 83]. Table 5.7 compares the weight of laboratory mice against 8 strains of wild mice. It is highly probable that the wild mice are a different species, so the observed differences may simply be differences by species, and not necessarily related to diet. Table 5.8 presents data from Brieger [1937] on the results of feeding rats 3 different types of raw diets. Unfortunately, Brieger [1937], as reported in Howell, provides comparison data only on raw-food diets, and does not provide data on cooked-food diets. Table 5.8 also has data from Donaldson [1924], but we don't know if the rats used by Donaldson are the same species or strain used by Brieger, hence cannot compare. Table 5.9 provides data from a variety of researchers on rat pancreas size. However, none of the studies cited are a raw-versus-cooked comparison that Howell says we need.

Thus the result of a close examination of the data in Howell is to conclude that it is a confused mess, and the data do not meet the criteria specified above. That is, none of the studies cited compares raw vs. cooked diets for the same species/strain of rats; also the species/strain used is not specified for some of the studies. Thus we note that the data presented by Howell do not support his conclusion.

Other logical/procedural problems with the experimental data cited. The approach of Howell to the above topic has a number of other problems. First, the laboratory rats used in some of the earlier papers cited by Howell may have been fed "raw grain" [Howell 1985, p. 77] as part of the diet provided them. The term "raw grain" might also include raw legumes, and it is well-known that the enzyme inhibitors in raw legumes can increase pancreas size in rats; Liener [1994] and Pusztai et al. [1995]. Hence any laboratory feed that included raw legumes might cause an increase in pancreas size.

Second, and of greater importance, are the following:

• It is well known that the digestive system in a wide variety of animals can and does change in size in reaction to changes in diet. This effect can occur rapidly, in as little as a few weeks (i.e., within the duration of most feeding studies). See Milton [1987] for references on this topic.

• Underlying all of Howell's discussion on pancreas size is the assumption that a larger pancreas is "bad" or "harmful" in some sense. However, Howell never provides a credible proof for this critical point.

Note: Neither Howell [1985] nor Howell [1946] include a reference list--yet another serious shortcoming--hence we cannot provide a citation for Brieger [1937] or Donaldson [1924], above.

COMMENT: The first remark is that the "proof" here is incomplete. The only way to complete it would be to take arctic animals to the lab and feed them an enzyme-free (but not vitamin-deficient) diet. Some animals might need germs (for other reasons than enzyme production), and others not.

The second remark is that, at that time, germ-free animals were still relatively new, and their special nutritional needs not well-known. Nowadays, they have been extensively studied and used [Wostmann 1996]. The nutritional requirements of germ-free animals differ from the normal ones for many reasons. (Germs, i.e., bacteria, can have various effects on digestive elements of the intestinal tract, on the physical conditions of the digestive tract, may synthesize certain B-vitamins, chelate certain vitamins or minerals, etc.) Lifespan of germ-free animals has gradually improved from the beginning of the 20th century until now, with a better understanding of their nutritional requirements. Nowadays, the core of the diet is maintained at 120°C (248°F) for at least 15 minutes, which inactivates all enzymes, no doubt. The resulting diet needs to be supplemented by high-quality protein and vitamins to keep the animals healthy.

In reality, germ-free animals, if properly fed, are healthier overall than their conventional counterparts [Wostmann 1996]. They have a considerably lower incidence of kidney disease, fewer solid tumors, live on average 6 months longer; and in general, spontaneous tumors occur somewhat less frequently in germ-free rats than in conventional ones. (To be more precise, by "conventional" is meant non-germ-free, but fed the same synthetic diet as the germ-free animals.) They also reproduce as successfully as their conventional counterparts.

Certainly, these comparisons tell little about whether animals fed a natural diet would be healthier or not, but at least two points are proved: (a) You can live reasonably well without enzymes, at least for a few generations; (b) It's not true that germs produce enzymes that are useful for animal health.

And of course, there is no reason to believe that the natural fate of animals should be to die peacefully, with all organs still functioning perfectly... Humans are idealistic, not Nature.

So, ironically, the crucial argument of Howell, which could have been considered as strong at his time, is reversed and proves that animals not receiving exogenous enzymes (from food or bacteria) aren't less healthy, and so food enzymes are not necessary to maintain good health (sure, sure, maybe the 100th generation will become sick... :-) ).

COMMENT: Here again, the unproven concept of enzyme potential is used, and asserted with no evidence offered. In older people, all body functions can be impaired, as well as mental functions. But no one will say that the "thinking potential" has been used up, and that we should exercise our brains less in order to keep the reserves of thoughts, or "thought potential" that we inherited at birth! Same remarks for enzyme secretion in disease, which is impaired because of the disease and not the other way around.

COMMENT: The logic of the author or the claim here is not apparent. Assuming for the moment it were true that an animal will die when completely deprived of pancreatic juice, it does not at all prove or even suggest that the pancreas isn't able to produce enough enzymes daily on an as-needed basis, as related to type of food eaten. All the above experiment tells one is that SOME pancreatic function is necessary to sustain life. No one argues that point. Beyond this it gives no further insight, and is beside the point in regard to Howell's enzyme theory about "saving" enzymes.

The pancreas secretes other critically important substances besides just digestive enzymes. Humans secrete a considerable amount of pancreatic juice every day (1.2 to 1.5 liters), which consists of more than just enzymes. Pancreatic juice consists of water, select digestive enzymes, sodium bicarbonate, and some salts. The pancreas also secretes important hormones, e.g., insulin and glucagon. For details, see Tortora and Anagostakos [1981, pp. 615, 626]. So the above experiment--by itself--cannot even tell us whether the death is caused by the loss of enzymes and not of something else in pancreatic juice, or if the death is due to physical factors unrelated to enzymes.

Reasoning is typically black-and-white. However, even if one were to assume for the sake of discussion that it is in fact the enzymes which are responsible, we are still left with the fact that total loss of a function or secretion is a black-and-white discontinuity (seized upon by black-and-white reasoning) that doesn't furnish us with any insight into the actual efficiencies or functional RANGE that an organ operates within under actual conditions.

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(Assessing the Arguments & Corollaries of the Theory of "Food Enzymes," cont.)

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