Study Indicates Prostate Cancer Is Reversible By Diet

According to the National Cancer Institute, each year in the U.S., 240,890 men get diagnosed with prostate cancer, and 33,720 men die from it.

According to the American Cancer Society,

"About 1 man in 6 will be diagnosed with prostate cancer during his lifetime. More than 2 million men in the United States who have been diagnosed with prostate cancer at some point are still alive today.

"Prostate cancer is the second leading cause of cancer death in American men, behind only lung cancer. About 1 man in 36 will die of prostate cancer."

I have a family history of prostate cancer, so I have a personal interest in prevention and remedy for this disease of civilization.

According to some people, whole grains and legumes cause or promote the diseases of civilization, including cancer.

If this disease is caused by eating grains and legumes, then any diet based on grains and legumes should promote cancer.  If you give men living with prostate cancer a diet rich in whole grains and legumes, you should see a promotion of the cancer.

My friend, Gordon Saxe, M.P.H., Ph.D., M.D., professor of medicine at U.C.S.D.,  has actually tested this hypothesis, albeit unintentionally.

Gordon has lead pilot research in which men with diagnosed with prostate cancer were taught to eat a diet consisting of whole grains, legumes, vegetables, fruits, nuts, and seeds, while eliminating animal  products, based on evidence [discussed here] that this dietary pattern may reduce the risk or progression of prostate cancer.

If whole grains and legumes promote prostate cancer then these men should have had an accelerated progression of their cancers.  However, in the first study, over six months, this intervention produced just the opposite effect:  a 100-fold reduction in the rate of rise of their disease, as measured by the rate of change in levels of prostate-specific antigen (PSA).  As stated by Saxe et al:

"The rate of PSA increase decreased in 8 of 10 men, while 3 had a decrease in absolute PSA. Results of the signed rank test indicated a significant decrease in the rate of increase in the intervention period (p = 0.01). Estimated median doubling time increased from 6.5 months (95% confidence interval 3.7 to 10.1) before to 17.7 months (95% confidence interval 7.8 to infinity) after the intervention. Nine of 10 participants in the study had reduction in the rate of rise of their PSA, a marker for progression of disease."

When 9 of 10 people respond in the very same way to an intervention, in this case with a reduction in rate of rise of PSA, this tends to suggest that the effect is no accident and most likely indicates a definite therapeutic effect of the intervention.

In the second study, involving 14 men, Saxe et al produced a similar result.  In this second study they explored the biological mechanisms involved:

"During the first 3 months of the intervention, as both median WHR and body weight declined significantly, the median rate of PSA rise not only declined but became negative, reflecting a slight reduction in absolute PSA and possibly disease regression in patients with absolute reductions. Conversely, during the second 3 months of the intervention, when median body weight increased (though not significantly), median PSA began to rise again, albeit more slowly than during the period prior to Baseline."

This second study suggested that weight-related metabolic changes may have mediated the reduction in rate of PSA increase.  In other words, the intervention resulted in a loss of body fat and concommitant metabolic changes related to reduction of body fatness, including an increase in sex hormone binding globulin, that influence prostate cancer.

"Assuming that the attenuation of PC progression was mediated by weight-related metabolic changes, a question arises as to what aspect of intervention brought about the observed reduction in adiposity. Earlier ⁵³, we described large increases during months 0–3 in intake of whole grains and vegetables, food groups which are fiber and water-rich, very low in fat, and therefore of low energy density. However, intake of these foods declined slightly during months 3–6. Weight loss during the first three months may possibly have resulted from replacing energy-rich foods with energy-poor foods, and the slight increase in body weight during the second three months may have resulted from a small degree of dietary recidivism." 

So this intervention, based on increasing intake of whole grains, legumes, etc., resulted in body fat reduction during the period when the subjects ate the most of these foods, and body weight increased during the period when these subjects ate less of these foods.  This clearly undermines the idea that diets rich in grains and legumes cause two of the major diseases of civilization, i.e. obesity and cancer.

Saxe et al consider the possibility that any diet that induces weight loss may reduce cancer progression.

"A second question that naturally arises regarding the reduction in adiposity is whether it matters, in terms of effects on prostate cancer progression, how it is achieved. One aspect of this question has to do with the preferred dietary strategy for reducing energy intake. Another facet regards whether it is more desirable to increase energy expenditure or decrease intake to achieve this end. Although our study and its findings did not address these issues, they remain important ones that warrant consideration in the planning and design of future behavioral approaches to the management of progressive PC. What can be said is that while both a plant-based diet and a high-protein, low-carbohydrate diet high in foods of animal origin (such as the popular Atkins diet) may both result in weight loss, the former is far more consistent with the dietary cancer prevention guidelines of various agencies (69).⁵⁴ "

Some people reject those cancer prevention guidelines of various agencies, which emphasize increased consumption of whole plant foods and decreased consumption of animal products, claiming that whole grains and legumes are the true causes of diseases of civilization.   These two studies, among others, weaken that claim. 

So far, the only studies I can find testing the effect of a low-carbohydrate diet on prostate cancer were done with mice, not men.  In this one, researchers from Duke Prostate Center fed mice with prostate cancer either a "Western" diet,  "low-fat high-carbohydrate" diet, or a zero-carbohydrate diet.  The results:

"Fifty-one days after injection [with xenograft tumors], NCKD mice tumor volumes were 33% smaller than Western mice (rank-sum, P = 0.009). There were no differences in tumor volume between low-fat and NCKD mice. Dietary treatment was significantly associated with survival (log-rank, P = 0.006), with the longest survival among the NCKD mice, followed by the low-fat mice."

I don't have access to the full text, but if done in a typical fashion, all diets would have been pellets made from isolated nutrients (e.g. casein, starch, sugar, etc.) so this can't tell us much about what would happen in humans if we compared a whole foods vegan diet (whole grains, legumes, vegetables, fruits, nuts, seeds) to a zero-carbohydrate diet (meat and fat only).  The effects of a casein-based zero-carbohydrate diet on mice might be very different from the effects of a meat-based zero-carbohydrate diet on humans.

In a second study, Masko et al fed mice diets containing 0, 10, or 20 percent carbohydrate and again injected them with prostate cancer cells.  As a 'control' they fed a group of mice a 12% fat diet, but they did not inject cancer cells into these mice--which to me means they weren't much of a control group, because they differed from the others not only in dietary composition but also in absence of tumor injection.

The full text of this study tells us the components of all diets:  corn oil, lard, milk fat, casein, dl-methionine, dextrine, maltodextrine, corn starch, sucrose, and isolated vitamins and minerals. 

In the low-fat arm, 72% of calories came from carbohydrate, and 50% of total calories came from sucrose, which means that about 25% of total calories came from refined fructose.  Meanwhile, in the 10% and 20% carbohydrate arms, all of the carbohydrate was provided in the form of corn starch. 

This makes me wonder again about diet composition in the other Duke University study cited above.  Were those mice on the low fat diet also eating a 50% sucrose/25% fructose diet?  If so, did this rig the study, intentionally or not, so that the low fat group would have more body fat and shorter lifespan than the zero-carbohydrate group? 

Moving on, all the mice got all of their protein from casein-plus-methionine, none ate any meat.  Most people eating low carbohydrate diets eat cooked meats, not isolated casein, as their main protein source.  Meat is nutritionally complex, and affected by cooking process, in ways that may result in it having a different effect on prostate cancer than casein-plus-methionine.  For example, unlike the casein-methionine mix fed to these mice, meat contains heme iron and if cooked at high heat, heterocyclic amines, all of which have been linked to prostate cancer causation or promotion [e.g. Sinha et al full text].  So it is not clear how a study of mice eating a low carbohydrate diet wherein casein is the main protein will apply to people eating low carbohydrate diets wherein cooked meat, poultry, and fish are the main protein sources.

Masko et al found that the survival rates of the mice in the 0, 10, and 20 percent carbohydrate groups were similar.  They liked this finding because, as they say, people find it extremely difficult to follow zero-carbohdyrate diets, so now they are ready to test the 20 percent carbohydrate diet on human prostate cancer patients. 

Masko et al also found that the mice in the 20% carbohydrate group had the lowest insulin level, about which they comment:

"It was unexpected that the lowest levels of insulin were observed in mice fed with 20% carbohydrate, but there are possible explanations for this phenomenon. First, there is always the possibility for a type I error in the analysis. Second, it is known that low-carbohydrate diets promote insulin sensitivity in animals (38) and humans (39, 40). Thus, it is possible that a diet containing a small amount of carbohydrates may actually improve insulin sensitivity compared with a diet completely lacking of carbohydrates."

Perhaps unknown to Masko et al, it is also 'possible' that a diet containing an even large amount of carbohydrate may actually improve insulin sensitivity compared to a diet with only 20% carbohydrate. In 1971, Brunzell et al [abstract only] evaluated the effect of increased dietary carbohydrate at the expense of fat in humans, both non-diabetic and mildly diabetic.  In the New England Journal of Medicine they reported that after feeding these subjects a diet providing 85 percent of energy as carbohydrate for 10 days,

"Fasting plasma glucose levels fell in all subjects and oral glucose tolerance (0 to 120-minute area) significantly improved ..... Fasting insulin levels also were lower on the high carbohydrate diet; however, insulin responses to oral glucose did not significantly change. These data suggest that the high carbohydrate diet increased the sensitivity of peripheral tissues to insulin."

 An diet supplying 85 percent of energy as carbohydrate is by necessity very low in fat, so perhaps Brunzell et al could have emphasized that this very low fat diet increased insulin sensitivity.  The mice of Masko et al that got the 20 percent carbohydrate diet had a lower fat intake than the mice on the zero-carbohydrate diet; rather than increasing carbohydrate being responsible for promoting insulin sensitivity, perhaps it is reducing fat (replacing it with starch) that does the trick. 

Anyway, the Masko et al study has a few features that make me skeptical that they will have similar results in humans.  I feel curious to see if their approach will have results as good as those found by Saxe et al.

Phytate Facts

Concerned about phytates in seed foods (nuts, seeds, grains, legumes) blocking mineral absorption and causing ill health?

You can relax.  Context matters. 

Consuming foods rich in ascorbate (vitamin C) with foods rich in phytate can cancel the negative effects of phytate on mineral absorption.[1, pdf]  Just eat some fruits and vegetables with foods that supply phytate.

Some studies have shown substantial degradation of phytate in the human gut (70-86%), indicating that humans adapt to diets high in phytate by increasing small intestinal production of phytase. [2 full text link, 3]

I have never seen any evidence that dietary phytate causes mineral deficiencies except in the context of overall poor quality diet, such as people attempting to live on diets composed entirely of unleavened grains and legume flours without adequate intake of vegetables, fruits, and other mineral sources.

If you live in a modern industrialized nation, when was the last time you had someone tell you that a physician diagnosed her with multiple mineral deficiencies caused by excessive dietary phytate?

I have never seen it.

Anticancer Effects of Phytates

Everything has a front and a back.

According to researchers from Linus Pauling Institute of Science and Medicine, phytates appear to have anticancer effects by binding excess minerals in tissues, depriving tumors of essential minerals.[4 pdf]

Vucenik and Shamsuddin discuss the anticancer properties of phytate in detail; all information and quotes remaining in this post come from their report in the Journal of Nutrition.[5 full text]

Almost all mammalian cells contain phytate in the inositol hexaphosphate (IP6) form and others with smaller numbers of phosphate groups (IP1-5).  When we ingest dietary phytate, intracellular levels of IP6 increase, and from this cells increase the levels of the other forms, which appear involved in "cellular signal transduction, regulation of cell function, growth, and differentiation."

Dietary phytate enters the blood stream and reaches tissues, including tumors, far from the gut.

Tumor cells take up phytate, probably by pinocytosis or receptor-mediated endocytosis.

Phytate inhibits malignant growth in human leukemic, colon cancer, breast cancer, cervical cancer, prostate cancer, and liver cancer cells.

"IP₆ inhibited the growth of all tested cell lines in a dose- and time-dependent manner. The growth of cells of hematopoietic lineage was inhibited: human leukemic hematopoietic cell lines, such as K-562 (26,27) and human normal and leukemic hematopoietic cells (27). The antiproliferative activity of IP₆ was further reported in human colon cancer HT-29 cells (28), estrogen receptor–positive and estrogen receptor–negative human breast cancer cells (32), cervical cancer (25), prostate cancer (15,33,34), and HepG2 hepatoma cell lines (31). IP₆ also inhibited the growth of mesenchymal tumors, murine fibrosarcoma (39), and human rhabdomyosarcoma (38)."

Phytate also causes malignant cells to mature and differentiate into normal cells:

"The potential of IP₆ to induce differentiation and maturation of malignant cells, often resulting in reversion to the normal phenotype, was first demonstrated in K-562 hematopoietic cells (26). IP₆ was further shown to increase differentiation of human colon carcinoma HT-29 cells (28,29), prostate cancer cells (33), breast cancer cells (32), and rhabdomyosarcoma cells (38)."

Phytates provide an intracellular antioxidant function by binding with iron, which suppresses formation of the most hazardous hydroxyl radicals:

"The antioxidant role of IP₆ is known and widely accepted; this function of IP₆ occurs by chelation of Fe³⁺ and suppression of ·OH formation (11). Therefore, IP₆ can reduce carcinogenesis mediated by active oxygen species and cell injury via its antioxidative function."

Phytate also stimulates the immune response and protects against carcinogen-induced depression of natural killer cell activity.

"Besides affecting tumor cells, IP₆ can act on a host by restoring its immune system. IP₆ augments natural killer cell activity in vitro and normalizes the carcinogen-induced depression of natural killer cell activity in vivo (59). "

Phytate only adversely affects malignant cells, not normal cells:

" The most important expectation of a good anticancer agent is for it to only affect malignant cells and not affect normal cells and tissues. That property was recently shown for IP₆. When the fresh CD34⁺ cells from bone marrow was treated with different doses of IP₆, a toxic effect (inhibition of the clonogenic growth or as cytotoxicity on liquid cultures) was observed that was specific to leukemic progenitors from chronic myelogenous leukemia patients but no cytotoxic or cytostatic effect was observed on normal bone marrow progenitor cells under the same conditions."

 This indicates that normal cells are adapted to phytate.  Of course, since phytate is abundant in the plant world and also present in almost every mammalian cell.

Phytate inhibits all of the several pathways supporting malignancy:

" From the behavior and characteristics of malignant cells, several principal pathways of malignancy have been established, such as proliferation, cell cycle progression, metastases and invasion, angiogenesis, and apoptosis; interestingly, IP₆ targets and acts on all of them."

 In one pilot clinical trial, six patients with advanced colorectal cancer (Dukes C and D) with multiple liver and lung metastasis received oral phytate plus chemotherapy.  One of the patients refused additional chemotherapy after one session and she was treated only with IP₆ plus inositol.  What happened?

"...her control ultrasound and abdominal computed tomography scan 14 mo after surgery showed a significantly reduced growth rate. A reduced tumor growth rate was noticed overall and in some cases a regression of lesions was noted."

Say again?  A simple, natural dietary ingredient reversed the progress of cancer!

Which reminds me:

"Pioneering experiments showing this novel anticancer feature of IP₆ were performed by Shamsuddin et al. (18–20), who were intrigued by the epidemiologic data indicating that only diets containing a high IP₆ content (cereals and legumes) showed a negative correlation with colon cancer." 

Most hunter-gatherer groups would have consumed significant phytate from nuts and seeds of various sorts, including legumes.

Dietary Phytate Safety
   
Vucenik and Shamsuddin agree that chronic phytate ingestion does not cause mineral deficiencies whether gotten from food or isolated form unless the overall diet lacks essential minerals:

"Some concerns have been expressed regarding the mineral deficiency that results from an intake of foods high in IP₆ that might reduce the bioavailability of dietary minerals. However, recent studies demonstrate that this antinutrient effect of IP₆ can be manifested only when large quantities of IP₆ are consumed in combination with a diet poor in oligoelements (60–63). A long-term intake of IP₆ in food (60,61) or in a pure form (64) did not cause such a deficiency in humans. Studies in experimental animals showed no significant toxic effects on body weight, serum, or bone minerals (Table 5) or any pathological changes in either male F344 or female Sprague-Dawley rats for 40 wk (40,51,52). Grases et al. (65) confirmed our findings and also reported that abnormal calcification was prevented in rats given IP₆."

 Phytate has many benefits:  

"In humans, IP₆ not only has almost no toxic effects, but it has many other beneficial health effects such as inhibition of kidney stone formation and reduction in risk of developing cardiovascular disease. IP₆ was administered orally either as the pure sodium salt or in a diet to reduce hypercalciuria and to prevent formation of kidney stones, and no evidence of toxicity was reported (64,65,79,80). A potential hypocholesterolemic effect of IP₆ may be very significant in the clinical management of hyperlipidemia and diabetes (75,76,81). IP₆ inhibits agonist-induced platelet aggregation (82) and efficiently protects myocardium from ischemic damage and reperfusion injury (83), both of which are important for the management of cardiovascular diseases. "

Perhaps avoiding and removing phytates from food doesn't serve your best interests?

Perhaps we evolved to consume significant amounts of phytates, and cancer is a disease facilitated by a dietary deficiency of phytates?

Legumes: Neolithic or Not?

Some people have suggested that legumes are a relatively ‘new’ food in human diets, introduced only with agriculture, discordant with human biology, and causes of disease.   Some have raised concerns about a number of secondary plant compounds in legumes, especially isoflavones considered phytoestrogens.

I have decided to view human evolution in the larger context of primate evolution, because we share so many characteristics with other primates and have a genome 98 percent similar to that of our nearest relative, the chimpanzee.  Since modern humans eat legumes, and humans share a common ancestor with chimps, if modern chimps eat legumes, this would suggest that probably the last common ancestor of humans and chimps also ate legumes.

So I decided to find out, do modern wild chimps eat legumes? 

It only took a few internet searches to find that, indeed, non-human primates, including chimps, consume legume seeds, leaves, and flowers.

The most remarkable of the literature I have so far come across on this topic is a paper published in the American Journal of Primatology by Shoeninger, Moore, and Sept, entitled “Subsistence Strategies of Two “Savanna” Chimpanzee Populations: The Stable Isotope Evidence.” [1 pdf]  In this paper, the authors report on Ugalla chimps, living “in open, grassy woodland habitats similar to those in which the last common ancestor of apes and humans probably lived.”  These chimps consumed a diet very rich in fresh legumes, estimated at 50% of total food consumption, certainly a level requiring some level of physiological adaptation. 

This puts fresh legumes in a different class from grains.  So far as I know, we have no evidence of chimps consuming any significant amounts of immature grass seeds (grains).

Green Peas.  Source: Ecosalon

Based on this type of evidence, it seems probable that fresh legumes were part of hominoid diets for millions of years before the advent of agriculture.  This would give plenty of time for hominoid physiology to become adapted to regular intake of fresh legumes and their phytochemical constituents, and also provide an evolutionary pathway to the domestication of legumes.

I know many people feel worried about isoflavones with phytoestrogen properties affecting sexual development, function, and fertility.   They have the idea that plants produce these compounds to disrupt the fertility of animals consuming them.

It is easy to think of the herbivore as the enemy of the plants it consumes, and vice versa, but grazing herbivores provide water, nitrogen, and minerals to plants via saliva, urine, and feces deposited in the field while grazing.  Herbivore hooves also knead and soften the soil.   The plants receive many needed services from their ‘enemies,’  not the least of which is a supply of carbon dioxide, without which they can’t live.  The herbivores need the nutrients and oxygen the plants produce.  Food plants and animals using them form a yin-yang pair, complementary and opposite, but if antagonistic, both sides fail.

If a plant slightly limits the fertility of an animal grazing upon it, this actually serves the animal species.  Sure, some individuals may complain because they don't get the litters they want, but by keeping the animal numbers within limits, this reduces the chance that the animal population will overshoot its resource base and crash, while also increasing the amount of food/nutrients available for each individual animal, increasing the quality of life for the grazier.  The plant helps the animal maintain a sustainable population size, and by grazing, the animal helps the plant maintain a sustainable population size.   In the big picture, this is synergism, not antagonism.

The synergism and mutuality of plant-animal nutrition relationships is especially evident in human interactions with plants.  When humans like a plant, usually because the plant helps them thrive and reproduce,  the people take on the task of feeding, protecting, and promoting the reproduction of that plant.  Humans help plants that help humans thrive, so plants that help humans have become among the dominant plant species on the planet.

When thinking about evolutionary plant-animal interactions, I feel it is important to realize that organisms adapt not only to ‘beneficial’ but also to challenging aspects of their habitats, if given enough time. 

Let’s assume that at some point in the past, some herbivores were grazing on plants rich in phytoestrogens.  Let’s also assume that, initially, the herd grazing on these plants does have reduced fertility.  Nevertheless, within the herbivore herd a range of susceptibility to the phytoestrogens’ effects on fertility.  That is, some of the animals may be rendered completely infertile, some will have reduced fertility in varying degrees, some will have no reduction in fertility, and it is possible that in some animals the increase of phytoestrogens will actually increase fertility. 

If this process continues for several generations, gradually the animal population will move toward adaptation to the isoflavones.  The animals resistant to the anti-fertility effects of the isoflavones will have more offspring than those not resistant.   Eventually, the entire herd will have resistance to the effects of the typically encountered levels of isoflavones.  

Now, let’s suppose that the mechanism of action of the isoflavones is to reduce hormone levels in the animals.  In this situation, the animals resistant to the anti-fertility effects of these phytochemicals will be those who have an endogenous production of hormones high enough to counter the negative effects of the phytoestrogens.  Over several generations, the evolutionary result will be a species adapted to a phytochemical drain on its endogenous hormone production by virtue of a higher endogenous output of hormones to compensate for the losses induced by the phytochemical.

Now, if you take this species off of the diet to which it is adapted, removing or greatly reducing the ‘hormone disrupting’ phytochemicals, the animal’s usual hormonal output might be excessive.  As a consequence, the animal might develop disorders due to excessive levels of its own hormones.  Adding the phytochemicals back to its diet will reduce those hormone levels, producing a more balanced physiology, because the animal is genetically adapted to a diet containing chemicals that ‘disrupt’ its hormones.   It may actually need the ‘hormone disrupters’ to maintain hormone balance. 

Edamame.  Source:  Dried-edamame.com

I suggest that this may provide part of an evolutionary explanation for the growing body of research suggesting that consumption of legumes and other plant foods containing phytoestrogens may have positive effects on human health. 

I discussed here some research that supports the idea that plant-rich diets and specific whole plant foods can reduce the excessive sex hormone levels present in premature menarche, premenstrual symptoms, menstrual pain, polycystic ovary syndrome, hirsutism, menopausal syndrome, and reproductive system (breast, ovarian, etc.) cancers in women.

Tham et al of the Stanford Center for Research in Disease Prevention and the Department of Medicine discuss the growing evidence for potential health benefits of dietary isoflavones and lignans, two types of phytoestrogens  including prevention of cardiovascular disease, promoting bone health, and regulating hormone levels across the life cycle, in both men and women, to prevent sex hormone-linked reproductive system cancers. [2] 

World-wide patterns of human population growth seem to lend little support to the idea that phytoestrogens make people infertile.  Historically, growth rates have been luxuriant in nations consuming more plant-based diets (India, China, Asia in general) rich in phytoestrogens. 

Legume proteins may also have unique benefits.  For example, multiple studies have shown that substituting soy protein for animal protein might improve kidney function in type II diabetics with nephropathy [3, 4, 5, 6, 7, 8].  This may not be a property unique to soy, but an effect of legume protein versus animal protein, due to legume proteins having a different ratio of amino acids.  It certainly does not indicate lack of adaptation to legume proteins. 

I find it hard to fit this data into an picture of human evolution that considers legumes discordant with human biology, but it makes sense in a view that includes legumes among human ancestral foods. 

 

Lignans are another type of phytoestrogen.  As shown in this table, lignans occur in fruits and vegetables as well as seeds, nuts, legumes, and grains.  Although the seeds typically have the highest concentrations, sweet potatoes, carrots, asparagus, and garlic have levels comparable to pinto beans, peanuts, and several grains. 

Legumes like clover naturally occur in grasslands, and farmers grow clover as part of their pastures and fodder for ruminants.   Consequently, products from either pasture- or grain/legume-finished animals also can contain phytoestrogens, although in lesser amounts than in plants.  Hence, human ancestors probably would have gotten exposed to these compounds through eating wild game meat as well as plants.

Of course, as with every other item we ingest, dose and context affects outcome.  Nature never delivered isoflavones in concentrated pills or isolated legume proteins, absent counter-balancing compound present in the whole foods, nor did it give isoflavone-rich soy formula (based on soy protein isolate) to human infants.  Obviously, substituting soy infant formula for human breast milk is discordant with human biology.  

Now on to one of America's favorite beans.  

Coffee Bean.  Source: Whos3d3n

Did you know that coffee supplies the same isoflavones found in soybeans, albeit in smaller amounts? 

"This paper reports the isoflavone contents of roasted coffee beans and brews, as influenced by coffee species, roast degree, and brewing procedure. Total isoflavone level is 6-fold higher in robusta coffees than in arabica ones, mainly due to formononetin. During roasting, the content of isoflavones decreases, whereas their extractability increases (especially for formononetin). Total isoflavones in espresso coffee (30 mL) varied from 40 μg (100% arabica) to 285 μg (100% robusta), with long espressos (70 mL) attaining more than double isoflavones of short ones (20 mL). Espressos (30 mL) prepared from commercial blends contained average amounts of 6, 17, and 78 μg of genistein, daidzein, and formononetin, respectively. Comparison of different brewing methods revealed that espresso contained more isoflavones (170 μg/30 mL) than a cup of press-pot coffee (130 μg/60 mL), less than a mocha coffee (360 μg/60 mL), and amounts similar to those of a filtered coffee cup (180 μg/120 mL)."

J. Agric. Food Chem., 2010, 58 (5), pp 3002–3007

Legumes in Hunter-Gatherer Diets

Did hunter-gatherers eat legumes?

According to Sigrid Leger, author of The Hidden Gifts of Nature, Bushmen ate the following legumes:

Wild Coffee Beans (Bauhinia petersiana):  "The seeds are edible and can be gathered from February until May. The pod is removed, the seeds are put into hot ash for a minute and are cooked in this way. After that the seeds can be eaten just as they are or they are pounded and then eaten."

Marama bean (Tylosema esculentum):  "The whole pod is put into hot ash for a short time and removed again. After having cooled down, the pods are opened, the skin of the seed is removed and the seed itself is eaten."

These examples appear to illustrate that the absence of pots and pans in the archaeological record does not serve as evidence that prehistoric people did not eat cereals or legumes.  Anyone who has eaten popcorn or peanuts might realize that people can eat grains and legumes roasted as an alternative to boiled.

According to Brand-Miller and Holt, Australian Aborigines also made use of legumes:

"Although seeds, particularly cereals (seeds of the family Gruminae) are thought to have played only a minor role in palaeolithic diets, they appeared to be important in the diet of at least some groups of Australian Aborigines (AA). Before European occupation, collection of seeds was widespread, particularly in arid areas. It was predominant in the grassland areas of Australia but also in the desert areas where acacia trees (wattle trees) yielded abundant seeds. Grindstones used for seed grinding have been found in many areas."

And:

"It appears that ~ 50 of the 800 species of Acacia (wattle trees) native to Australia were used by AA for food.  Despite the wattle being Australia’s national flower, the seeds are generally unknown to non-AA as food sources. But Acacia seeds are outstanding in their nutrient content, being much higher in energy, protein and fat than any cereal crop such as wheat and rice. Their composition more closely resembles that of the legume family to which the Acacias actually belong."

According to some, legumes are among the neolithic foods that cause disease because of their supposed discordance with human genetics, yet both !Kung and AA appeared to have a high immunity to modern diseases of affluence.