Although in overall form the human gut appears distinctly carnivorous, humans have one unusual feature for a carnivore: we have salivary glands that produce amylase, which has the the sole function of digesting starch. Since meat contains essentially no starch, this feature could not have arisen as an adaptation to an exclusive meat diet. It clearly represents an adaptation to starch consumption. Did this arise recently, in response to the Neolithic shift to cereal-based diets, or does it have deeper roots?
Meet AMY1
AMY1 is the gene that codes for the production of salivary amylase. Perry et al compared the AMY1 copy number variation humans from low-starch diet populations, humans from high-starch diet populations, and wild-born chimpanzees. They also examined the amount of nucleotide sequence divergence among the three AMY1 gene copies found in the human genome reference sequence.
The high-starch diet populations included Hadza hunter-gatherers and two agricultural groups, European Americans and Japanese. The low-starch diet populations included Yakut pastoralists and two rainforest hunter-gatherer groups, Biaka and Mbuti. The high-starch diet people carried a median of 7 and a mean of 6.72 copies of AMY1, in a range of 2 to 15 copies. The low-starch diet people carried a median of 5 and a mean of 5.44 copies of AMY1, and exhibited a range of 2 to 13 copies. Thus, AMY1 copy number correlated positively with diet.
When Perry et al examined 15 wild-born chimpanzees, they found evidence of only two diploid AMY1 copies. Thus, whereas the humans from high- and low- starch diet groups vary but the average human, regardless of high- or low-starch diet, has about 3 times as many copies of this gene as the chimpanzee. As a result, humans produce 6 to 8 times as much salivary amylase as chimpanzees.
Perry et al found a low amount of nucleotide sequence divergence among the three AMY1 gene copies found in the human genome reference sequence, which “implies a relatively recent origin that may be within the time frame of modern human origins.” Assuming that humans and chimps diverged from a common ancestor about 6 million years ago, they estimate that the increase in AMY copy number occurred within the last 200,000 years, the time period during which modern humans (H. sapiens sapiens) emerged.
This strongly suggests that starchy food has had a significant role in human diets for substantial time periods, starting in Paleolithic times. Most likely, this adaptation arose as an advantage in digestion of tubers, corms, and bulbs. It implies that these foods played a large enough role in human evolutionary diets to give a selective survival advantage to individuals who had extra copies of AMY1 (compared to chimps) and hence an enhanced ability to digest starch. I see no other way of explaining our unusual production of an otherwise useless salivary enzyme.
As I noted in The Garden of Eating, in 1996 anthropologist Melissa Darby, M.A., of Lower Columbia Research and Archaeology (Oregon) demonstrated that Northern Hemisphere paleolithic humans had access to arrowhead (Sagittaria latifolia) a prolific wetlands plant that produces a tuber very similar to the white potato. Pollen data indicates that this tuber —called “wapatos” by the Chinook tribe – thrived in the last Ice Age throughout North America, the North American Great Basin, Siberia, and Northern Europe – overlapping the time that during which Perry et al estimate that humans started showing extra copies of the AMY1 gene.
Darby has harvested approximately 5,418 calories per hour gathering wapatos from a knee-deep pond. The tuber is most abundant from late fall through spring, when other plant foods are scarce. People can eat these tubers without grinding or mashing, and they cook thoroughly in a bed of hot ashes in 10 minutes, no oven required. They keep fresh in a cool place, and also dried.
American Prairie Indian women also gathered and cultivate the starchy camas bulb. Darby says that a woman gathering camas could net 5,279 calories per hour. This would consist primarily of starch: nearly 1000 g of it.
Thus, we know that humans had access to tubers—I’ll call them primal potatoes—even during the Ice Ages. It seems fairly certain that we have descended from a long line of tuber-eaters extending back at least a quarter of a million years. I have more to say on this in my next post.
Sunday, August 30, 2009
Thursday, August 27, 2009
Primal Diet On A Shoestring
Nutritionally Complete, Inexpensive Low Carbohydrate Meal Plan
Some of the questions I received on a previous post regarding nutrient, particularly folate, delivery of a diet containing no vegetation prompted me to run a nutritionalysis to see if I could create a nutritionally compete zero carbohydrate meal plan.
Alas, so far I could not do so, even when I included chicken liver in the daily diet to provide folate (chicken liver has about 400 mcg folate per 4 ounce serving). Although liver is very nutrient dense, without nuts (source of trace minerals not so well supplied by meat) and produce, I could not get adequate levels of vitamin C, vitamin E, magnesium, manganese, or potassium.
So, I changed my approach to create a diet with minimal carbohydrate, yet supplying all required nutrients, and I added the requirement that the daily diet cost would fall below the USDA allotments for Supplemental Nutrition Assistance Plan, otherwise known as food stamps.
I wanted to include the latter requirement because when I watched Food Inc a few weeks ago, I did not like the part where they created a sad story around a family that supposedly could not afford to purchase good food in a grocery store, so felt compelled to purchase $1 meals at fast food restaurants twice daily. I knew that story was a pile of corn grits, so I decided to prove it.
I succeeded in all respects. I came up with the following, tailored to my own nutritional requirements.
Cost of food and supplements
This menu provides 2442 calories, 191.0 g of fat, 63.7 g of carbohydrate (21 g as fiber; 42 g net carbohydrate), and 126.2 g of protein. That's 69% fat, 21% protein, and 10% carbohydrate. Saturated fat is 32% of energy, polyunsaturated 8%, and monounsaturated 22%.
It provides 524 mg folate (31% more than the RDA), and exceeded the RDA or AI for all nutrients measured on FitDay except VT-D, calcium, magnesium, and potassium.
Regarding calcium, metabolic studies indicate that the RDA overestimates calcium requirements. Current data indicates that people maintain calcium balance with an average intake of 741 mg per day [1]. This plan provides 782 mg of calcium. Also, adding 3 tablespoons of well-made bone broth (see The Garden of Eating for a recipe) to each daily meal will cost virtually nothing and add 300 mg calcium to bring total to over 1000 mg.
Regarding magnesium, metabolic studies indicate that the RDA overestimates magnesium requirements. Current data indicates that people maintain magnesium balance on an average intake of 165 mg per day [2]. This plan provides 285 mg, exceeding the 165 mg by 50%.
Regarding potassium, this plan provides 3608 mg, 77% of the "adequate intake" defined by the Institute of Medicine. Add some vegetable scraps to the pot while preparing the bone broth, and the broth will provide the necessary additional potassium. Alternatively, adding 1.5 cups of cantaloupe or similar fruit will bring the potassium to 4233 mg, 90% of the AI -- close enough -- while still keeping the total digestible carbohydrate at about 60 g/d, and increasing cost of the menu by only about thirty cents, to $5.46.
To cover vitamin D and vitamin K2, I included supplements: VT-D 2000 IU, VT-K 1.5 mg. I get them from Complementary Prescriptions.
According to the USDA’s Fact Sheet on Resources, Income, and Benefits for the Supplemental Nutrition Assistance Program (SNAP), a household of 4 qualifies for a maximum monthly allotment of food assistance in the amount of $668, or $167 per person, which comes to $5.57 per day. So you will have ten cents left over!
Someone with lower caloric requirements would just eat smaller portions and of course has lower nutrient requirements. They would spend even less.
So I have just shown that even people on food stamps can eat a highly nutrient dense, meat-based, low carbohydrate diet, shopping in conventional supermarkets.
So the Food Inc people got it wrong. That family doesn't need to eat at fast food joints. They could follow my plan, the whole family would lose body fat, the father would lose his diabetes, they would stop needing dental repairs, and they would then have the money he spent on medications for upgrading the quality of their food.
P.S. If you like this post and want to see more like it, please consider making a small donation or a recurring subscription payment using the PayPal buttons in the right hand column. Fighting fallacies is a full time job I love to do, but I need support to continue doing it. Also consider sending a link to this post to all of your Facebook and other friends.
Notes
1. Source: Hunt CD and Johnson LK. Calcium requirements: new estimations for men and women by cross-sectional statistical analyses of calcium balance data from metabolic studies. American Journal of Clinical Nutrition, Vol. 86, No. 4, 1054-1063, October 2007.
2. Source: Hunt CD and Johnson LK. Magnesium requirements: new estimations for men and women by cross-sectional statistical analyses of metabolic magnesium balance data. American Journal of Clinical Nutrition, Vol. 84, No. 4, 843-852, October 2006.
Some of the questions I received on a previous post regarding nutrient, particularly folate, delivery of a diet containing no vegetation prompted me to run a nutritionalysis to see if I could create a nutritionally compete zero carbohydrate meal plan.
Alas, so far I could not do so, even when I included chicken liver in the daily diet to provide folate (chicken liver has about 400 mcg folate per 4 ounce serving). Although liver is very nutrient dense, without nuts (source of trace minerals not so well supplied by meat) and produce, I could not get adequate levels of vitamin C, vitamin E, magnesium, manganese, or potassium.
So, I changed my approach to create a diet with minimal carbohydrate, yet supplying all required nutrients, and I added the requirement that the daily diet cost would fall below the USDA allotments for Supplemental Nutrition Assistance Plan, otherwise known as food stamps.
I wanted to include the latter requirement because when I watched Food Inc a few weeks ago, I did not like the part where they created a sad story around a family that supposedly could not afford to purchase good food in a grocery store, so felt compelled to purchase $1 meals at fast food restaurants twice daily. I knew that story was a pile of corn grits, so I decided to prove it.
I succeeded in all respects. I came up with the following, tailored to my own nutritional requirements.
Cost of food and supplements
| Food | Quantity | Grocery | Unit cost $ | Cost $ |
| Beef | 8 ounces cooked | Food City | 1.99/lb | 1.00 |
| Butter | 8 tablespoons (112 g) | Food City | 2.59/lb | 0.63 |
| Pork Chop | 4 ounces cooked | Food City | .99/lb | 0.50 |
| Eggs | 4 large | Food City | 1.69/doz | 0.56 |
| Walnuts | 1 ounce (14 halves) | Sprouts | 4.99/lb | 0.31 |
| Turnip greens | 4 cups raw (1/2 cup cooked) (220 g) | Food City | 0.92/lb | 0.45 |
| Broccoli | 2 cups raw (1 cup cooked) (182 g) | Sprouts | 0.77/lb | 0.31 |
| Carrots | 2 cups raw (1 cup cooked) (256 g) | Sprouts | 0.59/lb | 0.33 |
| Peppers, red | 1 cup cooked | Sprouts | 0.77/each | 0.77 |
| Vitamin D3 | 2 x 1000 IU | Complementary Prescriptions | 13.95/250,0.06/1000 IU | 0.12 |
| Vitamin K2 | 1.5 mg | Complementary Prescriptions | 10.95/60, 0.18 ea | 0.18 |
| TOTAL | $5.16 |
This menu provides 2442 calories, 191.0 g of fat, 63.7 g of carbohydrate (21 g as fiber; 42 g net carbohydrate), and 126.2 g of protein. That's 69% fat, 21% protein, and 10% carbohydrate. Saturated fat is 32% of energy, polyunsaturated 8%, and monounsaturated 22%.
It provides 524 mg folate (31% more than the RDA), and exceeded the RDA or AI for all nutrients measured on FitDay except VT-D, calcium, magnesium, and potassium.
Regarding calcium, metabolic studies indicate that the RDA overestimates calcium requirements. Current data indicates that people maintain calcium balance with an average intake of 741 mg per day [1]. This plan provides 782 mg of calcium. Also, adding 3 tablespoons of well-made bone broth (see The Garden of Eating for a recipe) to each daily meal will cost virtually nothing and add 300 mg calcium to bring total to over 1000 mg.
Regarding magnesium, metabolic studies indicate that the RDA overestimates magnesium requirements. Current data indicates that people maintain magnesium balance on an average intake of 165 mg per day [2]. This plan provides 285 mg, exceeding the 165 mg by 50%.
Regarding potassium, this plan provides 3608 mg, 77% of the "adequate intake" defined by the Institute of Medicine. Add some vegetable scraps to the pot while preparing the bone broth, and the broth will provide the necessary additional potassium. Alternatively, adding 1.5 cups of cantaloupe or similar fruit will bring the potassium to 4233 mg, 90% of the AI -- close enough -- while still keeping the total digestible carbohydrate at about 60 g/d, and increasing cost of the menu by only about thirty cents, to $5.46.
To cover vitamin D and vitamin K2, I included supplements: VT-D 2000 IU, VT-K 1.5 mg. I get them from Complementary Prescriptions.
According to the USDA’s Fact Sheet on Resources, Income, and Benefits for the Supplemental Nutrition Assistance Program (SNAP), a household of 4 qualifies for a maximum monthly allotment of food assistance in the amount of $668, or $167 per person, which comes to $5.57 per day. So you will have ten cents left over!
Someone with lower caloric requirements would just eat smaller portions and of course has lower nutrient requirements. They would spend even less.
So I have just shown that even people on food stamps can eat a highly nutrient dense, meat-based, low carbohydrate diet, shopping in conventional supermarkets.
So the Food Inc people got it wrong. That family doesn't need to eat at fast food joints. They could follow my plan, the whole family would lose body fat, the father would lose his diabetes, they would stop needing dental repairs, and they would then have the money he spent on medications for upgrading the quality of their food.
P.S. If you like this post and want to see more like it, please consider making a small donation or a recurring subscription payment using the PayPal buttons in the right hand column. Fighting fallacies is a full time job I love to do, but I need support to continue doing it. Also consider sending a link to this post to all of your Facebook and other friends.
Notes
1. Source: Hunt CD and Johnson LK. Calcium requirements: new estimations for men and women by cross-sectional statistical analyses of calcium balance data from metabolic studies. American Journal of Clinical Nutrition, Vol. 86, No. 4, 1054-1063, October 2007.
2. Source: Hunt CD and Johnson LK. Magnesium requirements: new estimations for men and women by cross-sectional statistical analyses of metabolic magnesium balance data. American Journal of Clinical Nutrition, Vol. 84, No. 4, 843-852, October 2006.
Thursday, August 20, 2009
Phytochemical Fallacies?
[For those who already read the first version of this post, I made a mistake while editing and erased all the great commments :-(. But I made some improvements to the content anyway. :-)]
I used to believe that people would derive great benefits from a diet containing large amounts of fruits and vegetables because such foods would supply people with an abundance of “beneficial” phytochemicals. I had gotten this belief from my conventional nutrition education – you can find the claim promoted in most textbooks and popular books on nutrition. Consequently I consumed 15 or more servings of vegetables and fruits every day for many years, and advocated a “produce-dominated” diet in my last book.
However, as I integrated the concept of evolutionary nutrition and studied native diets and health in that context, I gradually came to realize that humans can live quite well without plant foods (witness the Eskimos, Nenet, Masai, and numerous other tribes). This of course led me to question the idea that people need daily doses of phytonutrients to maintain a semblance of health. After all, Eskimos had no cancer on their native diet, yet antioxidant rich vegetables and fruits played little or no role in their daily diets.
Epidemiology Not Impressive
If you examine the evidence frequently trotted out to support the frequent ingestion of phytochemicals from vegetables and fruits, you will notice that advocates of plant-dominated diets rely almost exclusively on epidemiological evidence.
For example, to support a recommendation for consumption of at least 400g of vegetables and fruits daily, the World Cancer Research Institute and the American Institute for Cancer Research cite 4500 epidemiological studies reviewed by 150 scientists as evidence for the cancer-preventive effects of vegetables and fruits.
Sounds impressive, but it does not establish that vegetables and fruits protect against cancer. These studies at most establish that people who have a higher intake of vegetables and fruits have less cancer than people who a lower intake of the same. Since people who have the habit of eating lots of produce very likely have higher income, or other habits that may also protect against cancer, like refraining from smoking, taking less alcohol, exercising regularly, getting sun exposure (vitamin D), or eating less sugar, we can’t conclude from these studies that their higher intake of produce is what is actually responsible for their reduced risk of cancer.
In science, clinical trials provide the best way to test a hypothesis. If we hypothesize that increased vegetable and fruit intake will provide health benefits to humans, our best evidence will come from studies where we get people to increase their consumption of vegetables and fruits, then measure outcomes, preferably hard endpoints like incidence of heart disease or cancer, but at least soft endpoints like changes in blood characteristics that we have reason to believe will influence health outcomes.
Clinical Trials
In clinical trials, it appears that increasing human intake of vegetables and fruits either may have little or no benefits, or could even cause injury.
As discussed by Stephan in his two part series The Diet-Heart Hypothesis: Oxidized LDL , we have good evidence to indicate that oxidized LDL causes atherosclerosis. Since vegetables and fruits supply lots of putative “antioxidants,” we could recommend increasing vegetables and fruits for prevention of heart disease if we could show that it would reduce oxidation of LDL.
Van het Hoff et al found increased intake of vegetables and fruits did raise serum levels of vitamin C and carotenoids (ie, {alpha}-carotene, ß-carotene, lutein, zeaxanthin, and ß-cryptoxanthin), but this did not result in reduced oxidation of LDL. They wrote:
“Despite the significant increases in plasma concentrations of vitamin C and carotenoids in the vegetable- and carotenoid-supplemented groups, the total antioxidant activity of plasma, measured as ferric-reducing ability, remained unchanged (Table 3). Furthermore, consumption of the diets supplemented with vegetables or carotenoids did not enhance protection of LDL against copper-induced oxidation ex vivo. Neither the changes in lag time before onset of oxidation nor the maximum rate of oxidation were significantly different from those found in the control group.”
In Changes in Dietary Fat Intake Alter Plasma Levels of Oxidized Low-Density Lipoprotein and Lipoprotein(a), Silaste et al report the results of feeding two diets to thirty-seven healthy women. Both diets contained a reduced amount of total and saturated fat, while one diet was low in vegetables and the other was high in vegetables, berries, and fruit.
As reported by Silaste et al, “During the low-fat, low-vegetable diet, the subjects consumed 2 portions of both fruit and vegetables daily. On the low-fat, high-vegetable diet, they consumed 4 to 5 portions of fruit or berries and 5 to 6 portions of vegetables.”
Regarding fat intake, “The total fat intake was 70 g per day at baseline and decreased to 56 g (low-fat, low-vegetable diet) and to 59 g (low-fat, high-vegetable diet). The saturated fat intake decreased from 28 g to 20 g and to 19 g, and the amount of polyunsaturated fat intake increased from 11 g to 13 g and to 19 g (baseline; low-fat, low-vegetable; low-fat, high-vegetable; respectively).”
What happened? “Surprisingly, we found that in response to the low-fat, low-vegetable and the low-fat, high-vegetable diets, the average plasma levels of OxLDL-EO6 increased compared with the baseline diet.” In fact, the median plasma OxLDL-EO6 –oxidized LDL—increased by 27% in response to the low-fat, low-vegetable diet and 19% in response to the low-fat, high-vegetable diet. Also, the Lp(a) concentration was increased by 7% and 9%, respectively.
The study design used a randomized crossover design for each of the study diets, which increased confidence in the conclusion that both of the interventions – cutting fat and increasing produce – resulted in increased oxidation of LDL.
To summarize the results of this study by Silaste et al:
1. Reducing saturated fat intake by 8 to 9 grams, and replacing it with 2 to 8 grams of polyunsaturates, resulted in an increase of 27% in oxidized LDL.
2. Taking this (#1) as a second base, increasing fruit and vegetable intake from four portions daily (low fat, low vegetable and fruit diet) to nine to eleven portions daily (low fat, high vegetable and fruit diet) countered the effect of increasing polyunsaturates, dropping the increase in oxidation of LDL from a 27% increase to a 19% increase compared to the "high fat" control diet.
3. Doubling fruit and vegetable intake did not completely counter the increased oxidation brought about by decreasing total and saturated fat intake and increasing polyunsaturated fat intake.
4. The group with the highest intake of fruits and vegetables (nine to eleven portions daily) had the greatest (9%) increase in Lp(a).
Research suggests that increased Lp(a) increases risk for coronary heart disease, cerebrovascular disease, atherosclerosis, thrombosis, and stroke. Marcovina et al found that vegetarian Bantus have 40% higher levels of Lp(a) than fish-eating Bantus. Combining these two studies (Marcovina and Silaste), we get the impression that eating more fish will decrease your Lp(a) levels and reduce your risk of coronary heart disease, cerebrovascular disease, atherosclerosis, thrombosis, and stroke, while eating nine to eleven servings of fruits and vegetables may increase your Lp(a) and very slightly increase your risk of those diseases!
In the WHEL trial, Pierce et al randomly assigned about 3000 women previously treated for early stage breast cancer to two groups: one received “a telephone counseling program supplemented with cooking classes and newsletters that promoted daily targets of 5 vegetable servings plus 16 oz of vegetable juice; 3 fruit servings; 30 g of fiber; and 15% to 20% of energy intake from fat” while the other received literature describing the "5-A-Day" dietary guidelines.
Over a four year period, they found that this intensive education resulted in increases in intake of fruits and vegetables and decreases in fat intake: “servings of vegetables, +65%; fruit, +25%; fiber, +30%, and energy intake from fat, −13%.” They measured plasma carotenoid concentrations and these validated changes in fruit and vegetable intake.
After 7.3 years of follow-up care, the two groups had almost identical invasive cancer incidence, 16.7% in the intervention group, and 16.9% in the control group. Increasing intake of produce appeared to have no effect on cancer recurrence despite changes in blood levels of antioxidants. It neither reduced nor increased the incidence of recurrence. Since the incidence of recurrence was the same in both groups, this leaves open the possibility that the intake of fruits and vegetables increased the risk of recurrence. Unfortunately, subjects in both arms of this study, so we can't tell if the intake of produce contributed to recurrence. They needed an arm with no intake of vegetables and fruits to find out whether fruits and vegetables might have had an adverse effect.
For another example, consider “Green tea extract only affects markers of oxidative status postprandially: lasting antioxidant effect of flavonoid-free diet.” This title tells all – a flavonoid-free diet produced a lasting antioxidant effect. The abstract reported: “Since no long-term effects of GTE [green tea extract] were observed, the study essentially served as a fruit and vegetables depletion study. The overall effect of the 10-week period without dietary fruits and vegetables was a decrease in oxidative damage to DNA, blood proteins, and plasma lipids, concomitantly with marked changes in antioxidative defence.”
So giving up fruits and vegetables for 10 weeks reduced oxidative damage to DNA, blood proteins, and plasma lipids; that means that eating fruits and vegetables increases damage to DNA, blood proteins, and plasma lipids.
How can that be?
For anyone convinced that flavonoids are just beneficial “antioxidants,” this evidence produces cognitive dissonance. How could eating vegetables and fruits possibly increase damage to DNA, blood protein, and blood lipids?
Now, taking an evolutionary tact, let us ask, why do plants produce flavonoids? Well, they provide photoprotection, necessary if you sit out in the sun all day.
But that's not all. Plants have no claws or teeth, nor can they run from predators, so they have chemical defenses instead. From a natural selection standpoint, any plant that produces and stores in its tissues chemicals that will injure, sterilize, or kill predators will have a marked selective reproductive advantage over less-equipped plants. Well, it turns out that flavonoids also function as pesticides!
In “Dietary pesticides (99.99% all natural)” Ames et al “estimate that Americans eat about 1.5 g of natural pesticides per person per day, which is about 10,000 times more than they eat of synthetic pesticide residues.” This natural pesticide intake includes compounds in coffee (caffeine, chlorogenic acid, neochlorogenic acid, caffeic acid), phenols (several hundred mg daily, in tea, berries, etc.), flavonoids and glucosinolates (another several hundred mg), potato and tomato toxins (a hundred mg), and saponins from legumes (peanuts included).
Naturally, they state, “The human intake of these toxins varies markedly with diet and would be higher in vegetarians.” Hmmm….food for thought.
Many people seek out “organic” foods to avoid pesticides. They may not know that plants grown “organically” actually have higher levels of these natural pesticides than plants grown conventionally. You will likely increase your total natural pesticide exposure by eating organic produce.
These natural phytochemicals don't appear benign – as Ames et al note, of the 52 of these natural pesticides have been tested in high-dose animal tests, 27 have proven carcinogenic, and these occur in many common foods. In isolation, in high enough doses, they have toxicity – and carcinogenicity – comparable to similar doses of synthetic chemicals.
Some will argue that the synergistic effect of multiple ingredients in plants reduces this toxicity. But I doubt that. Remember, the plants that survived evolution were those that either poisoned or created symbiotic relationships with predators. These chemicals may make plants excellent medicines -- many have antiviral, antibacterial, antifungal, and general antimicrobial effects, just what a plant needs to survive.
With this knowledge, you may no longer feel surprised that eating too many servings of vegetables and fruits – especially raw vegetables – might actually cause problems such as increased Lp(a), oxidized LDL, or damaged DNA. These natural pesticides might not kill you outright as they might an insect or worm, but they sure could cause digestive distress, cellular damage, or even neurological effects (like caffeine). You can learn more about that at Plant Poisons and Other Rotten Stuff.
The dose makes the poison. Most likely, we don't consume carcinogenic levels of these poisons when eating typical quantities of fruits and vegetables. Some hunter-gatherer tribes do eat substantial amounts of fruits and vegetables (wild types, which have even higher concentrations of poisons), yet remain free of cancer and heart disease. Significantly, hunter-gatherers tend to consume more fruits than vegetables. Fruits have lower toxin levels and enable a plant to work symbiotically with animals/predators to increase reproductive success.
Natural selection also favored the survival of plant predators (animals) that have the ability to detoxify these plant poisons. Our liver does this; but one must wonder, at what intake of produced -- especially high toxin vegetables like leaves -- does one start burdening the liver's detoxification systems?
In many cases, these poisons do have a bad taste (usually bitter) and adverse effects on the GI tract. Traditional cultures with plant based diets got around these toxins with cooking and other processing techniques. I consider unwise the modern raw-food vegetarian who does not follow their example.
I used to believe that people would derive great benefits from a diet containing large amounts of fruits and vegetables because such foods would supply people with an abundance of “beneficial” phytochemicals. I had gotten this belief from my conventional nutrition education – you can find the claim promoted in most textbooks and popular books on nutrition. Consequently I consumed 15 or more servings of vegetables and fruits every day for many years, and advocated a “produce-dominated” diet in my last book.
However, as I integrated the concept of evolutionary nutrition and studied native diets and health in that context, I gradually came to realize that humans can live quite well without plant foods (witness the Eskimos, Nenet, Masai, and numerous other tribes). This of course led me to question the idea that people need daily doses of phytonutrients to maintain a semblance of health. After all, Eskimos had no cancer on their native diet, yet antioxidant rich vegetables and fruits played little or no role in their daily diets.
Epidemiology Not Impressive
If you examine the evidence frequently trotted out to support the frequent ingestion of phytochemicals from vegetables and fruits, you will notice that advocates of plant-dominated diets rely almost exclusively on epidemiological evidence.
For example, to support a recommendation for consumption of at least 400g of vegetables and fruits daily, the World Cancer Research Institute and the American Institute for Cancer Research cite 4500 epidemiological studies reviewed by 150 scientists as evidence for the cancer-preventive effects of vegetables and fruits.
Sounds impressive, but it does not establish that vegetables and fruits protect against cancer. These studies at most establish that people who have a higher intake of vegetables and fruits have less cancer than people who a lower intake of the same. Since people who have the habit of eating lots of produce very likely have higher income, or other habits that may also protect against cancer, like refraining from smoking, taking less alcohol, exercising regularly, getting sun exposure (vitamin D), or eating less sugar, we can’t conclude from these studies that their higher intake of produce is what is actually responsible for their reduced risk of cancer.
In science, clinical trials provide the best way to test a hypothesis. If we hypothesize that increased vegetable and fruit intake will provide health benefits to humans, our best evidence will come from studies where we get people to increase their consumption of vegetables and fruits, then measure outcomes, preferably hard endpoints like incidence of heart disease or cancer, but at least soft endpoints like changes in blood characteristics that we have reason to believe will influence health outcomes.
Clinical Trials
In clinical trials, it appears that increasing human intake of vegetables and fruits either may have little or no benefits, or could even cause injury.
As discussed by Stephan in his two part series The Diet-Heart Hypothesis: Oxidized LDL , we have good evidence to indicate that oxidized LDL causes atherosclerosis. Since vegetables and fruits supply lots of putative “antioxidants,” we could recommend increasing vegetables and fruits for prevention of heart disease if we could show that it would reduce oxidation of LDL.
Van het Hoff et al found increased intake of vegetables and fruits did raise serum levels of vitamin C and carotenoids (ie, {alpha}-carotene, ß-carotene, lutein, zeaxanthin, and ß-cryptoxanthin), but this did not result in reduced oxidation of LDL. They wrote:
“Despite the significant increases in plasma concentrations of vitamin C and carotenoids in the vegetable- and carotenoid-supplemented groups, the total antioxidant activity of plasma, measured as ferric-reducing ability, remained unchanged (Table 3). Furthermore, consumption of the diets supplemented with vegetables or carotenoids did not enhance protection of LDL against copper-induced oxidation ex vivo. Neither the changes in lag time before onset of oxidation nor the maximum rate of oxidation were significantly different from those found in the control group.”
In Changes in Dietary Fat Intake Alter Plasma Levels of Oxidized Low-Density Lipoprotein and Lipoprotein(a), Silaste et al report the results of feeding two diets to thirty-seven healthy women. Both diets contained a reduced amount of total and saturated fat, while one diet was low in vegetables and the other was high in vegetables, berries, and fruit.
As reported by Silaste et al, “During the low-fat, low-vegetable diet, the subjects consumed 2 portions of both fruit and vegetables daily. On the low-fat, high-vegetable diet, they consumed 4 to 5 portions of fruit or berries and 5 to 6 portions of vegetables.”
Regarding fat intake, “The total fat intake was 70 g per day at baseline and decreased to 56 g (low-fat, low-vegetable diet) and to 59 g (low-fat, high-vegetable diet). The saturated fat intake decreased from 28 g to 20 g and to 19 g, and the amount of polyunsaturated fat intake increased from 11 g to 13 g and to 19 g (baseline; low-fat, low-vegetable; low-fat, high-vegetable; respectively).”
What happened? “Surprisingly, we found that in response to the low-fat, low-vegetable and the low-fat, high-vegetable diets, the average plasma levels of OxLDL-EO6 increased compared with the baseline diet.” In fact, the median plasma OxLDL-EO6 –oxidized LDL—increased by 27% in response to the low-fat, low-vegetable diet and 19% in response to the low-fat, high-vegetable diet. Also, the Lp(a) concentration was increased by 7% and 9%, respectively.
The study design used a randomized crossover design for each of the study diets, which increased confidence in the conclusion that both of the interventions – cutting fat and increasing produce – resulted in increased oxidation of LDL.
To summarize the results of this study by Silaste et al:
1. Reducing saturated fat intake by 8 to 9 grams, and replacing it with 2 to 8 grams of polyunsaturates, resulted in an increase of 27% in oxidized LDL.
2. Taking this (#1) as a second base, increasing fruit and vegetable intake from four portions daily (low fat, low vegetable and fruit diet) to nine to eleven portions daily (low fat, high vegetable and fruit diet) countered the effect of increasing polyunsaturates, dropping the increase in oxidation of LDL from a 27% increase to a 19% increase compared to the "high fat" control diet.
3. Doubling fruit and vegetable intake did not completely counter the increased oxidation brought about by decreasing total and saturated fat intake and increasing polyunsaturated fat intake.
4. The group with the highest intake of fruits and vegetables (nine to eleven portions daily) had the greatest (9%) increase in Lp(a).
Research suggests that increased Lp(a) increases risk for coronary heart disease, cerebrovascular disease, atherosclerosis, thrombosis, and stroke. Marcovina et al found that vegetarian Bantus have 40% higher levels of Lp(a) than fish-eating Bantus. Combining these two studies (Marcovina and Silaste), we get the impression that eating more fish will decrease your Lp(a) levels and reduce your risk of coronary heart disease, cerebrovascular disease, atherosclerosis, thrombosis, and stroke, while eating nine to eleven servings of fruits and vegetables may increase your Lp(a) and very slightly increase your risk of those diseases!
In the WHEL trial, Pierce et al randomly assigned about 3000 women previously treated for early stage breast cancer to two groups: one received “a telephone counseling program supplemented with cooking classes and newsletters that promoted daily targets of 5 vegetable servings plus 16 oz of vegetable juice; 3 fruit servings; 30 g of fiber; and 15% to 20% of energy intake from fat” while the other received literature describing the "5-A-Day" dietary guidelines.
Over a four year period, they found that this intensive education resulted in increases in intake of fruits and vegetables and decreases in fat intake: “servings of vegetables, +65%; fruit, +25%; fiber, +30%, and energy intake from fat, −13%.” They measured plasma carotenoid concentrations and these validated changes in fruit and vegetable intake.
After 7.3 years of follow-up care, the two groups had almost identical invasive cancer incidence, 16.7% in the intervention group, and 16.9% in the control group. Increasing intake of produce appeared to have no effect on cancer recurrence despite changes in blood levels of antioxidants. It neither reduced nor increased the incidence of recurrence. Since the incidence of recurrence was the same in both groups, this leaves open the possibility that the intake of fruits and vegetables increased the risk of recurrence. Unfortunately, subjects in both arms of this study, so we can't tell if the intake of produce contributed to recurrence. They needed an arm with no intake of vegetables and fruits to find out whether fruits and vegetables might have had an adverse effect.
For another example, consider “Green tea extract only affects markers of oxidative status postprandially: lasting antioxidant effect of flavonoid-free diet.” This title tells all – a flavonoid-free diet produced a lasting antioxidant effect. The abstract reported: “Since no long-term effects of GTE [green tea extract] were observed, the study essentially served as a fruit and vegetables depletion study. The overall effect of the 10-week period without dietary fruits and vegetables was a decrease in oxidative damage to DNA, blood proteins, and plasma lipids, concomitantly with marked changes in antioxidative defence.”
So giving up fruits and vegetables for 10 weeks reduced oxidative damage to DNA, blood proteins, and plasma lipids; that means that eating fruits and vegetables increases damage to DNA, blood proteins, and plasma lipids.
How can that be?
For anyone convinced that flavonoids are just beneficial “antioxidants,” this evidence produces cognitive dissonance. How could eating vegetables and fruits possibly increase damage to DNA, blood protein, and blood lipids?
Now, taking an evolutionary tact, let us ask, why do plants produce flavonoids? Well, they provide photoprotection, necessary if you sit out in the sun all day.
But that's not all. Plants have no claws or teeth, nor can they run from predators, so they have chemical defenses instead. From a natural selection standpoint, any plant that produces and stores in its tissues chemicals that will injure, sterilize, or kill predators will have a marked selective reproductive advantage over less-equipped plants. Well, it turns out that flavonoids also function as pesticides!
In “Dietary pesticides (99.99% all natural)” Ames et al “estimate that Americans eat about 1.5 g of natural pesticides per person per day, which is about 10,000 times more than they eat of synthetic pesticide residues.” This natural pesticide intake includes compounds in coffee (caffeine, chlorogenic acid, neochlorogenic acid, caffeic acid), phenols (several hundred mg daily, in tea, berries, etc.), flavonoids and glucosinolates (another several hundred mg), potato and tomato toxins (a hundred mg), and saponins from legumes (peanuts included).
Naturally, they state, “The human intake of these toxins varies markedly with diet and would be higher in vegetarians.” Hmmm….food for thought.
Many people seek out “organic” foods to avoid pesticides. They may not know that plants grown “organically” actually have higher levels of these natural pesticides than plants grown conventionally. You will likely increase your total natural pesticide exposure by eating organic produce.
These natural phytochemicals don't appear benign – as Ames et al note, of the 52 of these natural pesticides have been tested in high-dose animal tests, 27 have proven carcinogenic, and these occur in many common foods. In isolation, in high enough doses, they have toxicity – and carcinogenicity – comparable to similar doses of synthetic chemicals.
Some will argue that the synergistic effect of multiple ingredients in plants reduces this toxicity. But I doubt that. Remember, the plants that survived evolution were those that either poisoned or created symbiotic relationships with predators. These chemicals may make plants excellent medicines -- many have antiviral, antibacterial, antifungal, and general antimicrobial effects, just what a plant needs to survive.
With this knowledge, you may no longer feel surprised that eating too many servings of vegetables and fruits – especially raw vegetables – might actually cause problems such as increased Lp(a), oxidized LDL, or damaged DNA. These natural pesticides might not kill you outright as they might an insect or worm, but they sure could cause digestive distress, cellular damage, or even neurological effects (like caffeine). You can learn more about that at Plant Poisons and Other Rotten Stuff.
The dose makes the poison. Most likely, we don't consume carcinogenic levels of these poisons when eating typical quantities of fruits and vegetables. Some hunter-gatherer tribes do eat substantial amounts of fruits and vegetables (wild types, which have even higher concentrations of poisons), yet remain free of cancer and heart disease. Significantly, hunter-gatherers tend to consume more fruits than vegetables. Fruits have lower toxin levels and enable a plant to work symbiotically with animals/predators to increase reproductive success.
Natural selection also favored the survival of plant predators (animals) that have the ability to detoxify these plant poisons. Our liver does this; but one must wonder, at what intake of produced -- especially high toxin vegetables like leaves -- does one start burdening the liver's detoxification systems?
In many cases, these poisons do have a bad taste (usually bitter) and adverse effects on the GI tract. Traditional cultures with plant based diets got around these toxins with cooking and other processing techniques. I consider unwise the modern raw-food vegetarian who does not follow their example.
Saskatoon Circle Primitive Living Skills Gathering
I am so happy to be highlighting this Primitive Skills Gathering held near my home in the beautiful Methow Valley.
This gathering is focused on learning ancient crafts while enjoying community.
The class list is quite extensive and the cost is for the weekend is unheard of!
I'll be teaching several classes and hope to see you there!
http://www.saskatooncircle.blogspot.com/
Thursday, August 13, 2009
FDA on GMPs (Notes on a lecture by Roy Upton)
From Herbmentor.com
Good Manufacturing Practices and the
Community Herbalist
Written by Rosalee de la Foret
Based on notes from a lecture by
Roy Upton
Good Manufacturing Practices and the
Community Herbalist
Written by Rosalee de la Foret
Based on notes from a lecture by
Roy Upton
“In God we trust. Everyone else must show data.”
Robert Temple
Director, Office of Medical Policy, CDER, FDA
Many of you know that the FDA has issued new laws and mandates for the manufacturing of herbal products. However many of us community herbalists are confused about how these new regulations will affect us.
This article is a collection of notes taken from a lecture by Roy Upton for the American Herbalist Guild (AHG). Members of the AHG can access this lecture and the accompanying power point presentation for free on the AHG website. http://www.americanherbalistsguild.com/.
I originally wrote this article for Herbmentor.com
In researching this topic I am very grateful to Roy Upton for taking the time to understand these new laws and then to explain them to the herbal community.
First a brief history of the DSHEA (Dietary Supplement Health and Education Act)
In 1991 FDA threatened to remove the majority of herbal products from the market. The DSHEA (pronounced “de shay”) was the counter bill to keep herbal products on the market and was passed in 1994.
The passing of the DSHEA was one of the biggest defeats in FDA history. This resulted in the dietary supplement health and education act and the now the new Good Manufacturing Practices (GMPs), which are the topic of this article.
Labels
Besides setting up guidelines to allow herbal products to stay on the market he DSHEA also gave the right to make limited health claims on the product label. Before the DSHEA it was illegal to list any potential benefits.
A word about labels and nomenclature:
Herbs of Commerce is the primary source of herb nomenclature. By law, all herbal products must be labeled with a complete ingredients list. Herbs can be listed with the common name, but it has to be the common name that corresponds to the Latin name in the Herbs of Commerce. Of course, botanical names are always the most accurate.
FDA reasoning on the necessity of the GMPs
GMPs were instated because herbal products were considered to need more regulation than conventional foods, but less than what was mandated for drugs.
The FDA gave a compliance timeline for the GMPs based on the size of the company. If a company had more than 500 employees, they needed to comply before June 2008. If they had less than 500 employees, but more than 20 they needed to comply before June 25th 2009. If a company has less than 20 employees, the date for compliance is set for June 25th 2010. So, in the end this applies to everything from the largest companies to the smallest of companies. The one exception is a Native American herbalist on a reservation under the sovereign treaty of their tribe.
Herbal products are licensed as a dietary supplement, which is a sub category of food. Herbal products include capsules, alcohol extracts, syrups, tablets, or any herbal product intended for oral consumption.
Salves, lotions and balms for soothing purposes are regulated as cosmetics.
Liniments, bolus, suppositories, nasal sprays, or other products similar to these are considered a drug.
Whole plant herbs are listed as food. So, if you are a wildcrafter or a farmer who grows herbs you have to adhere to food GMP policies.
If you make herbal products, you have to adhere to dietary supplement guidelines. If claims are made on herbal products to “cure” a disease then they are then considered a drug and fall under different regulations. This is why it’s important not to make medical claims on products.
So what are Good Manufacturing Practices?
GMPs are a set of policies that encompass everything from the buildings where the herbal products are made (such as plumbing, pest control, water supply, and equipment) to the processes of receiving ingredients, processing, handling, testing, manufacturing, bottling, labeling, cleaning, personnel, and documentation.
Under the new GMPs there is a written procedure for everything that must be done in the manufacturing of herbal products. There are then regulations to ensure that there are people overseeing that the procedures are being followed correctly and then further personnel to ensure they are doing their job correctly.
Larger companies are already legally required to adhere to these policies. However, it’s small herbal products business owners that will be most affected by these mandates.
GMPs are aimed to ensure:
• Authentication
• Purity
• Quality
• Consistency
• Documentation
• Traceability
• Accountability
They are for the prevention of:
• Adulteration
• Contamination
• Sophistication
→ (Leading to public health problems like ecoli outbreaks of spinach for example.)
The goals of the GMPs are hard to argue against. Who doesn’t want to know their herbs are pure and not adulterated with unknown herbs or contaminated with heavy metals? In recent history alone there have been several problems of herbs (especially herbs shipped from overseas) that have been adulterated with plant material. This adulteration has been anywhere from benign to life threatening.
These problems can arise because of the unfortunate reality that in modern times the general public gets their herbal knowledge from the herbal marketplace, not from the herbalist. Currently many naturopathic doctors and some herbalists depend on large manufacturing companies to distribute herbs. Many times these large companies (especially overseas, certainly in north America as well) are out for the bottom line and do not have policies set in place to determine correct ID of a plant and prevent adulteration. When someone receives plants in capsules, or liquid extracts how do they know what that plant really is? GMPs are supposedly put forth to ensure authentication of the herbs and therefore public safety in this arena.
It would be all but impossible for a community herbalist or small herbal products business to follow the GMPs.
The AHG and American Herbal Pharmacopeia both commented to the FDA that herbal practitioners should be exempted from GMPs because they would not be able to follow the same guidelines set forth for larger companies.
The FDA disagreed:
“We decline to exempt herbalist practitioners from the proposed rule. If an herbalist practitioner introduces or delivers for introduction into interstate commerce, a dietary ingredient or dietary supplement, that practitioner must use the same good manufacturing practices as other manufacturers to ensure that their clients receive dietary supplements that are not adulterated. The risks of adulteration are not eliminated just because the practitioner is an herbalist.
Therefore, we decline to exempt “herbalist'' practitioners who manufacture dietary ingredients and dietary supplements. Herbalist practitioners who introduce or deliver for introduction into interstate commerce, a dietary ingredient or dietary supplement, are manufacturers who must meet CGMPs.”
However, in the end the FDA acquiesced to a degree by saying they chose to exercise their regulatory discretion by not forcing practitioners to adhere to GMPs, although they still have the right to do so if they feel the need.
There was one stipulation however, which said for an herbal practitioner to avoid FDA scrutiny when selling their herbal wares they must have a direct personal consultation with the person buying their herbal products.
This means that if you are an herbal practitioner and you have a client that you consult with prior to selling them an herbal product then you are not outright expected to follow the GMPs.
However, if you are an herbal practitioner or a small herbal products company and you sell products at the farmer’s market or online then you would be expected to be in compliance with the GMPs. It is suggested then, if you are selling at the local market, or at a conference, and you do not follow the GMPs that you have a mini consultation prior to selling the product.
So how often does the FDA persecute small herbal companies or herbal practitioners? It’s not entirely common and historically the FDA most often goes after the products that claim to cure disease, especially if the word “cancer” is used. However it is important to note that herbalists have had the FDA come knocking on their door.
It’s also important to note that the FDA maintains the right to enforce GMPs on herbal practitioners, they are just not choosing to do so at this time.
Upton says this will most likely continue until a patient makes a claim that they were injured because of a practitioner’s product. At that point the FDA will have the political motivation to step in and will most likely do so.
Another important note is that regulatory discretion does not extend to the use or trade of prescribing of unsafe products. The question is how will the FDA define “unsafe products”. Herbalists using drop dosage herbs like Aconite will certainly raise eyebrows. However herbs like skullcap could also be worrisome because of historical adulterations of this herb. So the question of “unsafe products” is something to be aware of.
So how can we avoid the attention of the FDA and ensure our products are safe? Upton urges practitioners who manufacture their herbal products for clients to have some sort of quality assurances so that the FDA does not feel the need to enforce their regulations.
The potential of the repercussions of the FDA stepping in to stop community herbalists manufacturing their own products would be disastrous. We can imagine that there would be a big outcry and a legal battle would ensue, however, Upton points out that it is far better to prevent this by enacting some basic principles.
Of course our motivation for quality assurance is not just for the FDA, but also to maintain safety for our clients.
The first step is to ensure the identity of the plants that we buy or pick for our herbal products. By FDA standards you are required to perform at least one test to ensure the identity of the original plant material.
To do these tests you can use the most sophisticated analytical instruments out there. Your nose, tongue, and brain.
That’s right organoleptic testing is considered legit by the FDA, if you can correctly identify a plant by it’s genus and species and prove this through documentation. So, if you can only identify the genus, but not the species by your own senses, then this would not qualify as adequate testing.
So how do we go about doing this?
The best scenario is that the plant ID is confirmed at the growing site and accompanied by some type of identification/affidavit. Most companies or wild crafters don’t do this, which is why the manufacturer (or you) has to do further testing. If you are able to get this from your herbal supplier, this is ideal. It is recommended to keep this documentation on file in case there are any questions.
Since the above scenario is not always an option Upton suggests that practitioner herbalists who make their own products need to know how to correctly botanically key the plants we use down to the genus AND species. In order to do this herbalists need to be botanically trained and Upton recommends keeping the records of this training on file.
Of course as the herbs are more processed it is harder to know what it is. Organoleptic testing (again through sight, taste, smell, etc) can easily be done when receiving a whole fresh plant. But this becomes considerably more difficult the more a plant is processed. Whether it is dried, dried cut and sifted, or even powdered or extracted.
The good news is that as herbalists we will be served in honing our organoleptic skills.
Upton gives the following basic guidelines of what one should know intimately about the plants we are working with. (Also in the original lecture he gives a good amount of information on organoleptic testing procedures.)
• Size: length, width, diameter, thickness, etc.
• Shape: conical (carrot), cylindrical (astragalus), tear-shaped (tuber), entire, serrate, etc.
• Color: address differences in intensities, growth stage, variegation
• Taste: sweet, salty, pungent, bitter, bland, astringent, etc.
• Smell: Aromatic, hay-like, pleasant, unpleasant; intensity
• Texture: smooth, rough, wrinkled, corky, oily, hairy, etc.
• Fracture: complete, incomplete, fibrous, brittle, etc.
• Grades: Most specific for Chinese herbs; applicable to western and ayurvedic herbs as well.
• Adulterants: Understand how to differentiate between closely related adulterating species
• Relative purity
He also recommends that we keep a plant pressing of each herb that we use in our products. So if we wildcraft our herbs or if we buy our herbs fresh we press these plants are label them clearly including:
Name of plant
Where is was collected
Unique id #
Signature of the person who performed the ID
This should be done each time a new batch is procured/harvested. (Herbmentor members can use the search feature on the home page to find a video on how to make your own herb press.)
Upton says that each time you make an herbal product you should hold that plant in your hand and ask yourself if you can prove through documentation of your own testing that it is a certain genus and species.
Besides ensuring the genus and species of a plant and documenting the identification procedures (as outlined above) the FDA also requires that herbalists:
• Assess quality
• Prevent contamination and mix-up
Quality
The FDA defines quality as follows
“Quality means that the dietary supplement consistently meets the established specifications for identity, purity, strength and limits on contaminates and has been manufactured, packaged, labeled and held under conditions to prevent adulteration.”
Prevent contamination and mix-up
Including things like heavy metal contamination or adulteration with different plants.
Of course wild crafting our own plants or purchasing plants directly from the herbal farmer will be easier to identify the plant with certainty. Buying dried herbal materials from middle-man companies will prove to be much harder to identify with 100% certainty.
Upton urges herbalists to question these companies about their own testing procedures. For example if you are buying powdered Ashwagandah whose origin is in India you will want to question that company on a couple of key points.
1. What testing did the company do to determine this powder is indeed Ashwagandah? If it is a plant that has historically been adulterated with other plant material, what tests did they do to determine that it has not been adulterated?
2. What tests were performed to ensure that this batch of plant material does not have contamination problems like high levels of lead?
If the company you are buying from cannot provide testing to ensure these qualities for the health of yourself and your clients you will want to consider a better source.
The FDA aside, it just makes good sense to know you are dealing with pure quality herbs in which to make your quality herbal products.
One more consideration: Upton also points out that if you manufacture an herbal product for which there is a known common adulterant then identity testing alone is not sufficient. In this case there must be a negative test to assure there is a limit or specification that assures freedom from the adulterant.
Examples of potential adulterants in the American market
• Ginkgo extracts spiked with pure flavonoids
• Plantain potentially adulterated w/ digitalis
• Hoodia adulterated with prickly pear
• Skullcap adulterated with the potential hepatotoxin germander (Teucrium)
So, to re-cap on what all this means.
Larger herbal product companies are already legally required to follow the GMPs that have been put forth by the FDA. Herbal companies with less than 20 employees will be required to follow suit in June 2010. If you are the owner of a small herbal company you will need to know and understand all the GMPs set forth by the FDA.
It seems to me that small herbal products businesses, especially those selling their wares online and to a larger general audience will be the most impacted from these GMPs. It seems likely that many of these quality businesses will close since they will not be able to financially continue their small operation while having to adhere to the many policies put forth in the GMPs. I would love to see a discussion from these small business owners who know more about the actual GMPs and how this will be affecting them.
Herbal practitioners who sell their own herbal products to people after a personalized consultation are not currently obligated to follow the GMPs set forth for larger companies who sell to the general public without a consultation. However, it is a good practice to follow certain guidelines and documentation to ensure you know the products you are selling contain high quality herbs that have not been adulterated or contaminated and that you can prove this if your herbal products are ever brought into question. This may include being personally familiar with the plants in order to test them organoleptically yourself, or being knowledgeable enough about chemical testing to hold third person suppliers responsible for ensuring quality from the grower/wildcrafter.
Upton covers the issue of common adulterations, and other topics much more in-depth in his lecture that can be found on the AHG website. The entirety of this article was written based on that lecture and I highly recommend those wanting more information to refer to it for deeper understanding. A heartfelt thanks goes out to Roy Upton for providing us with a better understanding of these new regulations.
American Herbal Pharmacopoeia®
PO Box 66809
Scotts Valley, CA
95067 US
Tel: 831-461-6318
FAX: 831-475-6219
email: ahpadmin@herbal-ahp.org
Website: www.herbal-ahp.org
PO Box 66809
Scotts Valley, CA
95067 US
Tel: 831-461-6318
FAX: 831-475-6219
email: ahpadmin@herbal-ahp.org
Website: www.herbal-ahp.org
Fiber Fallacies
Do you eat vegetables and fruits to get the “benefits” of fiber?
You might feel surprised to learn that not one experimental study has proven any beneficial effect or human requirement for fiber.
In terms of requirement, facts prove humans do not need fiber in the diet.
First, human breast milk contains no fiber, and infants have normal, healthy bowel function when exclusively breast fed – which by the way provides them with a high fat diet. In contrast, if fed high fiber foods, infants can experience colic due to accumulation of gas causing bloating of the intestine.
Second, several primitive groups, such as Inuit and Chukchi, eat or ate fiber-free diets and have or had no signs of illness, such as “constipation,” appendicitis, diverticular disease, or colorectal cancer commonly attributed to so-called fiber deficiency.
In fact, experimental studies (not epidemiological, which establish nothing) show high fiber intake to damage the gut and promote colon cell abnormalities.
“Disruption-Induced Mucus Secretion: Repair and Protection” explains how fiber damages the gut wall. The authors suggest this damage is “good” but Michael Eades has a different take on it in A Cautionary Tale of Mucus Fore and Aft.
Many people think eating a high fiber diet will prevent colon cancer; but we not only have no proof or even weak evidence that ingestion of fiber prevents colon cancer, on the contrary we have experimental evidence indicating that diets high in fermentable fibers actually increase colonic cell proliferation of the type that leads to cancer.
Lupton et al reported that a diet high in fermentable fiber increased cecum size and large intestine length, and reduced pH and stimulated cell proliferation, in rat colons. [J. Nutr. 118: 840-845, 1988.]
Jacobs and Lupton found that when they fed rats a high fiber diet based on either oat bran, pectin, or guar, the yield of proximal colonic adenocarcinomas increased by 4.5 to 5 times over the fiber free level. [Cancer Research 46, 1727-1734, April 1986]
Mandir, Englyst, and Goodlad found that when they fed mice fiber in the form of bran or apple pomace, both fibers significantly increased cell proliferation, number of polyps, and tumor burden born by the mice. Both fibers increased polyp diameter, bran by 243% and apple fiber by 150%. [British Journal of Nutrition (2008), 100, 711–721]
Generally, diets high in fiber make the feces softer and looser. A study by Inoue et al found “Soft or loose feces increased the risk for all subsites of colorectal cancer, particularly in female rectum cancer (odds ratio [OR] = 4.5)” [Cancer Causes Control 1995 Jan;6(1):14-22.]. Although epidemiological studies generally don’t carry much weight, when the odds ratio goes above 2.0, the association carries more weight. This finding of a greater than 4 fold increased risk of colorectal cancer in people with soft or loose stools suggests that high intake of fermentable fiber may promote cancer in humans as well as rats.
In their article “Fiber and colorectal diseases: Separating fact from fiction” published in the World Journal of Gastroenterology [2007 August 21; 13(31): 4161-4167], Tan and Seow-Choen review the physiological effects of fiber ingestion and evidence for beneficial effects of fiber. The facts include:
1. Fiber has no nutritive value. For this reason, of all carbohydrates, I would say that fiber perhaps most deserves the title “carbage.”
2. Fiber demonstrates antinutritive effects – blocking the absorption of essential nutrients. Another reason to put it in the junk food pile.
3. People eating high fiber diets demonstrate a greater risk of excessively long colons and a higher incidence of megacolon and volvulus (strangulated colon). This suggests that high fiber intake has a negative effect on colonic transit, actually facilitating impaction.
4. High fiber intake promotes bacterial growth and fermentation, which produces hydrogen, methane and carbon dioxide, causing cramps, bloating, and distension, all of which injure the colon.
5. Contrary to the predictions of Burkitt, Trowel, and other fiber fanatics, we have no evidence that increased fiber intake reduces diverticular disease; on the contrary “the incidence of diverticulosis and complications of diverticular disease have been increasing in the West despite increase in dietary fiber intake.”
6. We have no evidence that a human must have daily bowel evacuation of feces to maintain health of any body structure, colon included.
The volume and frequency of feces evacuation simply reflects how much indigestible matter you eat. The more carbage you eat, the more carbage you evacuate. On the other hand, if you eat a low residue diet – e.g. meat only – you may evacuate rather infrequently, simply because you don’t have any carbage to clear out.
On a side note, the larger and softer your stool, the more toilet paper you need to clean yourself. Who knows how many forests we can save by cutting down on fiber intake?
7. High fiber diets do not make it easier to evacuate. On the contrary, by increasing the bulk of the stool, a high fiber diet can make defecation more difficult, since the passage way out has a rather small diameter. Which leads to the next point….
8. People suffering from hemorrhoids and anal fissures should avoid high fiber diets. The large caliber of fiber rich stools contributes to straining on defecation, promoting hemorrhoids, and “Passage of large bulky stools will also result in direct trauma from stretching of the anal mucosa leading to anal fissures.”
In conclusion, fiber does not provide any of the benefits claimed for it, and has a number of deleterious effects rarely mentioned. I have experienced several of those ill effects first hand, most extremely when I ate a low-fat, high carbohydrate grain-bean-and-vegetable based diet, and to a much lesser degree when eating a plant-dominated hunter-gatherer style containing several pounds of produce daily. In the past year I have progressively reduced my intake of fibrous foods and so far I can say that every time I have cut down my carbage intake, my gut health has improved.
You might want to try it yourself.
You might feel surprised to learn that not one experimental study has proven any beneficial effect or human requirement for fiber.
In terms of requirement, facts prove humans do not need fiber in the diet.
First, human breast milk contains no fiber, and infants have normal, healthy bowel function when exclusively breast fed – which by the way provides them with a high fat diet. In contrast, if fed high fiber foods, infants can experience colic due to accumulation of gas causing bloating of the intestine.
Second, several primitive groups, such as Inuit and Chukchi, eat or ate fiber-free diets and have or had no signs of illness, such as “constipation,” appendicitis, diverticular disease, or colorectal cancer commonly attributed to so-called fiber deficiency.
In fact, experimental studies (not epidemiological, which establish nothing) show high fiber intake to damage the gut and promote colon cell abnormalities.
“Disruption-Induced Mucus Secretion: Repair and Protection” explains how fiber damages the gut wall. The authors suggest this damage is “good” but Michael Eades has a different take on it in A Cautionary Tale of Mucus Fore and Aft.
Many people think eating a high fiber diet will prevent colon cancer; but we not only have no proof or even weak evidence that ingestion of fiber prevents colon cancer, on the contrary we have experimental evidence indicating that diets high in fermentable fibers actually increase colonic cell proliferation of the type that leads to cancer.
Lupton et al reported that a diet high in fermentable fiber increased cecum size and large intestine length, and reduced pH and stimulated cell proliferation, in rat colons. [J. Nutr. 118: 840-845, 1988.]
Jacobs and Lupton found that when they fed rats a high fiber diet based on either oat bran, pectin, or guar, the yield of proximal colonic adenocarcinomas increased by 4.5 to 5 times over the fiber free level. [Cancer Research 46, 1727-1734, April 1986]
Mandir, Englyst, and Goodlad found that when they fed mice fiber in the form of bran or apple pomace, both fibers significantly increased cell proliferation, number of polyps, and tumor burden born by the mice. Both fibers increased polyp diameter, bran by 243% and apple fiber by 150%. [British Journal of Nutrition (2008), 100, 711–721]
Generally, diets high in fiber make the feces softer and looser. A study by Inoue et al found “Soft or loose feces increased the risk for all subsites of colorectal cancer, particularly in female rectum cancer (odds ratio [OR] = 4.5)” [Cancer Causes Control 1995 Jan;6(1):14-22.]. Although epidemiological studies generally don’t carry much weight, when the odds ratio goes above 2.0, the association carries more weight. This finding of a greater than 4 fold increased risk of colorectal cancer in people with soft or loose stools suggests that high intake of fermentable fiber may promote cancer in humans as well as rats.
In their article “Fiber and colorectal diseases: Separating fact from fiction” published in the World Journal of Gastroenterology [2007 August 21; 13(31): 4161-4167], Tan and Seow-Choen review the physiological effects of fiber ingestion and evidence for beneficial effects of fiber. The facts include:
1. Fiber has no nutritive value. For this reason, of all carbohydrates, I would say that fiber perhaps most deserves the title “carbage.”
2. Fiber demonstrates antinutritive effects – blocking the absorption of essential nutrients. Another reason to put it in the junk food pile.
3. People eating high fiber diets demonstrate a greater risk of excessively long colons and a higher incidence of megacolon and volvulus (strangulated colon). This suggests that high fiber intake has a negative effect on colonic transit, actually facilitating impaction.
4. High fiber intake promotes bacterial growth and fermentation, which produces hydrogen, methane and carbon dioxide, causing cramps, bloating, and distension, all of which injure the colon.
5. Contrary to the predictions of Burkitt, Trowel, and other fiber fanatics, we have no evidence that increased fiber intake reduces diverticular disease; on the contrary “the incidence of diverticulosis and complications of diverticular disease have been increasing in the West despite increase in dietary fiber intake.”
6. We have no evidence that a human must have daily bowel evacuation of feces to maintain health of any body structure, colon included.
The volume and frequency of feces evacuation simply reflects how much indigestible matter you eat. The more carbage you eat, the more carbage you evacuate. On the other hand, if you eat a low residue diet – e.g. meat only – you may evacuate rather infrequently, simply because you don’t have any carbage to clear out.
“Infants on breast feeding are known to be able to go for long periods of time without any bowel movement. This is because the breast milk is thoroughly absorbed with minimal residue. Therefore, if an individual has a low residue diet and therefore less frequent bowel movements simply because there is less faecal material to evacuate, this is not pathological.”
“In other words, the more fiber one ingests, the more faeces one will have to evacuate. By the mass effect of the formation of more faecal material, there will be a resultant increase in frequency of evacuation. By increasing fiber intake, stool frequency and faecal weight will be correspondingly increased. However, this is a classic case of rubbish in, rubbish out only.”
On a side note, the larger and softer your stool, the more toilet paper you need to clean yourself. Who knows how many forests we can save by cutting down on fiber intake?
7. High fiber diets do not make it easier to evacuate. On the contrary, by increasing the bulk of the stool, a high fiber diet can make defecation more difficult, since the passage way out has a rather small diameter. Which leads to the next point….
8. People suffering from hemorrhoids and anal fissures should avoid high fiber diets. The large caliber of fiber rich stools contributes to straining on defecation, promoting hemorrhoids, and “Passage of large bulky stools will also result in direct trauma from stretching of the anal mucosa leading to anal fissures.”
In conclusion, fiber does not provide any of the benefits claimed for it, and has a number of deleterious effects rarely mentioned. I have experienced several of those ill effects first hand, most extremely when I ate a low-fat, high carbohydrate grain-bean-and-vegetable based diet, and to a much lesser degree when eating a plant-dominated hunter-gatherer style containing several pounds of produce daily. In the past year I have progressively reduced my intake of fibrous foods and so far I can say that every time I have cut down my carbage intake, my gut health has improved.
You might want to try it yourself.
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