How to Treat Polycystic Ovary Syndrome (PCOS) with Diet

Given the role that oxidant free radicals are thought to play in aging and disease, one reason fruits and vegetables may be so good for us is that they contain antioxidant compounds. As you can see at 0:20 in my video Benefits of Marjoram for Polycystic Ovary Syndrome (PCOS), different vegetables and herbs have different antioxidant content. When making a salad, for example, spinach, arugula, or red leaf lettuce may provide twice the antioxidants as butterhead lettuce, and choosing purple cabbage over green, or red onions over white can also boost the salad’s antioxidant power.

Fresh herbs are so powerful that even a small amount may double or even quadruple the antioxidant power of the entire meal. For instance, as you can see at 0:50 in my video, the total antioxidants in a simple salad of lettuce and tomato jump up by adding just a tablespoon of lemon balm leaves or half a tablespoon of oregano or mint. Adding marjoram, thyme, or sage not only adds great flavor to the salad, but effectively quadruples the antioxidant content at the same time, and adding a little fresh garlic or ginger to the dressing ups the antioxidant power even more.

Herbs are so antioxidant-rich that researchers decided to see if they might be able to reduce the DNA-damaging effects of radiation. Radioactive iodine is sometimes given to people with overactive thyroid glands or thyroid cancer to destroy part of the gland or take care of any remaining tumor cells after surgery. For days after the isotope injection, patients become so radioactive they are advised not to kiss or sleep close to anyone, including their pets, and if they breathe on a phone, they’re advised to wipe it “carefully” or cover it “with an easily removed plastic bag.” Other recommendations include “avoid[ing] splatter of radioactive urine,” not going near your kids, and basically just staying away from others as much as possible.

The treatment can be very effective, but all that radiation exposure appears to increase the risk of developing new cancers later on. In order to prevent the DNA damage associated with this treatment, researchers tested the ability of oregano to protect chromosomes of human blood cells in vitro from exposure to radioactive iodine. As you can see at 2:25 in my video, at baseline, about 1 in 100 of our blood cells show evidence of chromosomal damage. If radioactive iodine is added, though, it’s more like 1 in 8. What happens if, in addition to the radiation, increasing amounts of oregano extract are added? Chromosome damage is reduced by as much 70 percent. Researchers concluded that oregano extract “significantly protects” against DNA damage induced by the radioactive iodine in white blood cells. This was all done outside the body, though, which the researchers justified by saying it wouldn’t be particularly ethical to irradiate people for experimental research. True, but millions of people have been irradiated for treatment, and researchers could have studied them or, at the very least, they could have just had people eat the oregano and then irradiate their blood in vitro to model the amount of oregano compounds that actually make it into the bloodstream.

Other in vitro studies on oregano are similarly unsatisfying. In a comparison of the effects of various spice extracts, including bay leaves, fennel, lavender, oregano, paprika, parsley, rosemary, and thyme, oregano beat out all but bay leaves in its ability to suppress cervical cancer cell growth in vitro while leaving normal cells alone. But people tend to use oregano orally—that is, they typically eat it—so the relevance of these results are not clear.

Similarly, marjoram, an herb closely related to oregano, can suppress the growth of individual breast cancer cells in a petri dish, as you can see at 3:53 in my video, and even effectively whole human breast tumors grown in chicken eggs, which is something I’ve never seen before. Are there any clinical trials on oregano-family herbs on actual people? The only such clinical, randomized, control study I could find was a study on how marjoram tea affects the hormonal profile of women with polycystic ovary syndrome (PCOS). The most common cause of female fertility problems, PCOS affects up to one in eight young women and is characterized by excessive male hormones, resulting in excess body or facial hair, menstrual irregularities, and cysts in one’s ovaries that show up on ultrasounds.

Evidently, traditional medicine practitioners reported marjoram tea was beneficial for PCOS, but it had never been put to the test…until now. Drinking two daily cups of marjoram tea versus a placebo tea for one month did seem to beneficially affect the subjects’ hormonal profiles, which seems to offer credence to the claims of the traditional medicine practitioners. However, the study didn’t last long enough to confirm that actual symptoms improved as well, which is really what we care about.

Is there anything that’s been shown to help? Well, reducing one’s intake of dietary glycotoxins may help prevent and treat the disease. Over the past 2 decades there has been increasing evidence supporting an important contribution from food-derived advanced glycation end products (AGEs)…[to] increased oxidative stress and inflammation, processes that play a major role in the causation of chronic diseases,” potentially including polycystic ovary syndrome (PCOS). Women with PCOS tend to have nearly twice the circulating AGE levels in their bloodstream, as you can see at 0:33 in my video Best Foods for Polycystic Ovary Syndrome (PCOS). 

PCOS may be the most common hormonal abnormality among young women in the United States and is a common cause of infertility, menstrual dysfunction, and excess facial and body hair. The prevalence of obesity is also higher in women with PCOS. Since the highest AGE levels are found in broiled, grilled, fried, and roasted foods of “mostly animal origin,” is it possible that this causal chain starts with a bad diet? For instance, maybe eating lots of fried chicken leads to obesity, which in turn leads to PCOS. In that case, perhaps what we eat is only indirectly related to PCOS through weight gain. No, because the same link between high AGE levels and PCOS was found in lean women as well.

“As chronic inflammation and increased oxidative stress have been incriminated in the pathophysiology [or disease process] of PCOS, the role of AGEs as inflammatory and oxidant mediators, may be linked with the metabolic and reproductive abnormalities of the syndrome.” Further, the buildup of AGE inside polycystic ovaries themselves suggests a potential role of AGEs contributing to the actual disease process, beyond just some of its consequences.

RAGE is highly expressed in ovarian tissues. The receptor in the body for these advanced glycation end products, the “R” in RAGE, is concentrated in the ovaries, which may be particularly sensitive to its effect. So, AGEs might indeed be contributing to the cause of PCOS and infertility.

Does this mean we should just cut down on AGE-rich foods, such as meat, cheese, and eggs? Or hey, why not come up with drugs that block AGE absorption? We know AGEs have been implicated in the development of many chronic diseases. Specifically, food-derived AGEs play an important role because diet is a major source of these pro-inflammatory AGEs. Indeed, cutting down on these dietary glycotoxins reduces the inflammatory response, but the “argument is often made that stewed chicken would be less tasty than fried chicken…” Why not have your KFC and eat it, too? Just take an AGE-absorption blocking drug every time you eat it to reduce the absorption of the toxins. What’s more, it actually lowers AGE blood levels. This oral absorbent drug, AST-120, is just a preparation of activated charcoal, like what’s used for drug overdoses and when people are poisoned. I’m sure if you took some ipecac with your KFC, your levels would go down, too.

There’s another way to reduce absorption of AGEs, and that’s by reducing your intake in the first place. It’s simple, safe, and feasible. The first step is to stop smoking. The glycotoxins in cigarette smoke may contribute to increased heart disease and cancer in smokers. Then, decrease your intake of high-AGE foods, increase your intake of foods that may help pull AGEs out of your system, like mushrooms, and eat foods high in antioxidants, like berries, herbs, and spices. “Dietary AGE intake can be easily decreased by simply changing the method of cooking from a high dry heat application to a low heat and high humidity…” In other words, move away from broiling, searing, and frying to more stewing, steaming, and boiling.

What we eat, however, may be more important than how we cook it. At 4:00 in my video, I include a table showing the amounts of AGEs in various foods. For instance, boiled chicken contains less than half the glycotoxins of roasted chicken, but even deep-fried potatoes have less than boiled meat. We can also eat foods raw, which doesn’t work as well as for blood pudding, but raw nuts and nut butters may contain about 30 times less glycotoxins than roasted, and we can avoid high-AGE processed foods, like puffed, shredded, and flaked breakfast cereals.

Why does it matter? Because study after study has shown that switching to a low-AGE diet can lower the inflammation within our bodies. Even just a single meal high in AGEs can profoundly impair our arterial function within just two hours of consumption. At 4:54 in my video, you can see the difference between a meal of fried or broiled chicken breast and veggies compared with steamed or boiled chicken breast and veggies. Same ingredients, just different cooking methods. Even a steamed or boiled chicken meal can still impair arterial function, but significantly less than fried or broiled.

“Interestingly, the amount of AGEs administered [to subjects] during the HAGE [high-AGE] intervention was similar to the average estimated daily intake by the general population,” who typically follow the standard American diet. This is why we can decrease inflammation in people by putting them on a low-AGE diet, yet an increase in inflammation is less apparent when subjects switch from their regular diet to one high in AGEs. Indeed, they were already eating a high-AGE diet with so many of these glycotoxins.

Do we have evidence that reducing AGE intake actually helps with PCOS? Yes. Within just two months, researchers found differences from subjects’ baseline diets switched to a high-AGE diet and then to a low-AGE diet, with parallel changes in insulin sensitivity, oxidative stress, and hormonal status, as seen at 5:54 in my video. The take-home learning? Those with PCOS may want to try a low-AGE diet, which, in the study, meant restricting meat to once a week and eating it only boiled, poached, stewed, or steamed, as well as cutting out fast-food-type fare and soda.

What if instead of eating steamed chicken, we ate no meat at all? Rather than measuring blood levels, which vary with each meal, we can measure the level of glycotoxins stuck in our body tissues over time with a high-tech device that measures the amount of light our skin gives off because AGEs are fluorescent. And, not surprisingly, this turns out to be a strong predictor of overall mortality. So, the lower our levels, the better. The “one factor that was consistently associated with reduced [skin fluorescence]: a vegetarian diet.” This “suggests that a vegetarian diet may reduce exposure to preformed dietary AGE…potentially reduc[ing] tissue AGE,” as well as chronic disease risk


What’s so great about antioxidants? See my videos:

Just how many antioxidants do we need? Check out:

For a few simple tips on how to quickly boost the antioxidant content of your food with herbs and spices, see my video Antioxidants in a Pinch.

I touched on the benefits of spearmint tea for PCOS in Enhancing Athletic Performance with Peppermint. Another sorely under-recognized gynecological issue is endometriosis, which I discuss in How to Treat Endometriosis with Seaweed.

Because of AGEs, I no longer toast nuts or buy roasted nut butters, which is disappointing because I really enjoy those flavors so much more than untoasted and unroasted nuts. But, as Dr. McDougall likes to say, nothing tastes as good as healthy feels. For more on why it’s important to minimize our exposure to these toxic compounds, see:

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

 

 

The Role of Meat and Dairy in Triggering Type 1 Diabetes

Type 1 diabetes “arises following the autoimmune destruction of the insulin-producing pancreatic β [beta] cells…[and] is most often diagnosed in children and adolescents, usually presenting with a classic trio of symptoms” as their blood sugars spike: excessive thirst, hunger, and urination. They need to go on insulin for the rest of their lives, since their own immune systems attacked and destroyed their ability to produce it. What would cause our body to do such a thing? I examine this in my video, Does Paratuberculosis in Milk Trigger Type 1 Diabetes?

Whatever it is, it has been on the rise around the world, starting after World War 2. “Understanding why and how this produced the current pandemic of childhood diabetes would be an important step toward reversing it.” A plausible guess is “molecular mimicry, whereby a foreign antigen (bacterial or viral) provokes an immune response, which cross-reacts” with a similar-looking protein on our pancreas such that when we attack the bug, our own organ gets caught in the cross-fire. Given this, what pancreatic proteins are type 1 diabetics self-attacking? In the 1980s, a protein was identified that we came to realize in the 1990s looked an awful lot like a certain mycobacterial protein. Mycobacteria are a family of bacteria that cause diseases like tuberculosis and leprosy, and, in one study, all newly diagnosed type 1 diabetic children were found to have immune responses to this mycobacterial protein. This didn’t make any sense as incidence of type 1 diabetes has been going up in the industrialized world, whereas TB and leprosy rates have gone down. However, there is one mycobacterial infection in farm animals that has shot up with the industrialization and globalization of animal agriculture: paratuberculosis (paraTB), which causes Johne’s disease in animals. Paratuberculosis is now recognized as a global problem for the livestock industry.

Weren’t there a dozen or so studies suggesting that “cow’s milk exposure may be an important determinant of subsequent type 1 diabetes” in childhood? Indeed. After putting two and two together, an idea was put forward in 2006: Could mycobacterium paratuberculosis from cattle be a trigger for type 1 diabetes? The idea was compelling enough for researchers put it to the test.

They attempted to test the association of Mycobacterium avium paratuberculosis (MAP), the full name for the bug, with type 1 diabetes by testing diabetics for the presence of the bacteria in their blood. Lo and behold, most of the diabetic patients tested positive for the bug, compared to only a minority of the healthy control subjects. This evidence of MAP bacteria in the blood of patients with type 1 diabetes “might provide an important foundation in establishing an infectious etiology,” or cause, for type 1 diabetes. “These results also might possibly have implications for countries that have the greatest livestock populations and high incidence of MAP concurrent with the highest numbers of patients with” diabetes, like the United States.

Johne’s is the name of the disease when farm animals get infected by MAP. The reason diabetes researchers chose to look at Sardinia, an island off the coast of Italy, is because paratuberculosis is present in more than 50 percent of Sardinian herds. Surpassing that, though, is the U.S. dairy herd. According to a recent national survey, 68 percent of the U.S. dairy herd are infected with MAP, especially those cattle at big, industrial dairies, as you can see at 3:33 in my video. Ninety-five percent of operations with more than 500 cows came up positive. It’s estimated the disease costs the U.S. industry more than a billion dollars a year.

How do people become exposed? “The most important routes of access of MAP to the [human] food chain appear to be contaminated milk, milk products and meat” from infected cattle, sheep, and goats. MAP or MAP DNA has been detected in raw milk, pasteurized milk, infant formula, cheese, ice cream, muscle and organ tissues, and retail meat. We know paraTB bacteria survive pasteurization because Wisconsin researchers bought hundreds of pints of retail milk off store shelves from three of the top U.S. milk-producing states and tested for the presence of viable, meaning living, MAP bacteria. They found that 2.8 percent of the retail milk tested came back positive for live paraTB bacteria, with most brands yielding at least one positive sample. If paraTB does end up being a diabetes trigger, then “these findings indicate that retail milk [in the United States] would need to be considered as a transmission vector.” Why hasn’t the public heard about this research? Perhaps because the industry is not too keen on sharing it. Indeed, according to an article in the Journal of Dairy Science: “Fear of consumer reaction…can impede rational, open discussion of scientific studies.”

Not only is MAP a serious problem for the global livestock industry, but it also may trigger type 1 diabetes, given that paraTB bacteria have been found in the bloodstream of the majority of type 1 diabetics tested who presumably are exposed through the retail milk supply as the bacteria can survive pasteurization. But what about the meat supply? MAP has been found in beef, pork, and chicken. It’s an intestinal bug, and unfortunately, “[f]aecal contamination of the carcass in the abattoir [slaughter plant] is unavoidable…” Then, unless the meat is cooked well-done, it could harbor living MAP.

In terms of meat, “ground beef represents the greatest potential risk for harboring MAP…[as] a significant proportion originates from culled dairy cattle,” who may be culled because they have paratuberculosis. These animals may go straight into the human food chain. There also exists greater prevalence of fecal contamination and lymph nodes in ground meat, and the grinding can force the bacteria deep inside the ground beef burger. As such, “given the weight of evidence and the severity and magnitude of potential human health problems, the precautionary principle suggests that it is time to take actions to limit…human exposure to MAP.” At the very least, we should stop funneling animals known to be infected into the human food supply.

We know that milk exposure is associated with type 1 diabetes, but what about meat? As I discuss in my video Meat Consumption and the Development of Types 1 Diabetes, researchers attempted to tease out the nutritional factors that could help account for the 350-fold variation in type 1 diabetes rates around the world. Why do some parts of the world have rates hundreds of times higher than others? Yes, the more dairy populations ate, the higher their rates of childhood type 1 diabetes, but the same was found for meat, as you can see at 2:07 in my video. This gave “credibility to the speculation that the increasing dietary supply of animal protein after World War II may have contributed to the reported increasing incidence of type 1 diabetes…” Additionally, there was a negative correlation—that is, a protective correlation that you can see at 2:26 in my video—between the intake of grains and type 1 diabetes, which “may fit within the more general context of a lower prevalence of chronic diseases” among those eating more plant-based diets.

What’s more, the increase in meat consumption over time appeared to parallel the increasing incidence of type 1 diabetes. Now, we always need to be cautious about the interpretation of country-by-country comparisons. Just because a country eats a particular way doesn’t mean the individuals who get the disease ate that way. For example, a similar study looking specifically at the diets of children and adolescents between different countries “support[ed] previous research about the importance of cow’s milk and [other] animal products” in causing type 1 diabetes. But, the researchers also found that in countries where they tended to eat the most sugar, kids tended to have lower rates of the disease, as you can see at 3:18 in my video. This finding didn’t reach statistical significance since there were so few countries examined in the study, but, even if it had and even if there were other studies to back it up, there are countless factors that could be going on. Maybe in countries where people ate the least sugar, they also ate the most high fructose corn syrup or something. That’s why you always need to put it to the test. When the diets of people who actually got the disease were analyzed, increased risk of type 1 diabetes was associated with milk, sugar, bread, soda, eggs, and meat consumption.

In Sardinia, where the original link was made between paraTB and type 1 diabetes, a highly “statistically significant dose-response relationship” was found, meaning more meat meant more risk, especially during the first two years of children’s lives. So, “[h]igh meat consumption seems to be an important early in life cofactor for type 1 diabetes development,” although we needed more data.

The latest such study, which followed thousands of mother-child pairs, found that mothers eating meat during breastfeeding was associated with an increased risk of both preclinical and full-blown, clinical type 1 diabetes by the time their children reached age eight. The researchers thought it might be the glycotoxins, the AGEs found in cooked meat, which can be transferred from mother to child through breastfeeding, but they have learned that paratuberculosis bacteria can also be transferred through human breast milk. These bacteria have even been grown from the breast milk of women with Crohn’s disease, another autoimmune disease linked to paraTB bacteria exposure.


For a deeper discussion of other possibilities as to why cow’s milk consumption is linked to this autoimmune destruction of insulin production, see Does Casein in Milk Trigger Type 1 Diabetes? and Does Bovine Insulin in Milk Trigger Type 1 Diabetes?.

If we don’t drink milk, though, what about our bone health? See my videos Long-Term Vegan Bone Health and Is Milk Good for Our Bones?.

The vast majority of cases of diabetes in the United States are type 2, though. Ironically, meat may also play a role there. See my videos Why Is Meat a Risk Factor for Diabetes? and How May Plants Protect Against Diabetes? for more information.

For more on the links between milk and diabetes, see my videos Does Casein in Milk Trigger Type 1 Diabetes? and Does Bovine Insulin in Milk Trigger Diabetes?. What about treating and preventing diabetes through diet? Check out How Not to Die from Diabetes and How to Prevent Prediabetes from Turning Into Diabetes.

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

Foods to Avoid to Help Prevent Diabetes

We’ve known that being overweight and obese are important risk factors for type 2 diabetes, but, until recently, not much attention has been paid to the role of specific foods. I discuss this issue in my video, Why Is Meat a Risk Factor for Diabetes?

A 2013 meta-analysis of all the cohorts looking at the connection between meat and diabetes found a significantly higher risk associated with total meat consumption––especially consumption of processed meat, particularly poultry. But why? There’s a whole list of potential culprits in meat: saturated fat, animal fat, trans fats naturally found in meat, cholesterol, or animal protein. It could be the heme iron found in meat, which can lead to free radicals and iron-induced oxidative stress that may lead to chronic inflammation and type 2 diabetes, or advanced glycation end (AGE) products, which promote oxidative stress and inflammation. Food analyses show that the highest levels of these so-called glycotoxins are found in meat—particularly roasted, fried, or broiled meat, though any foods from animal sources (and even high fat and protein plant foods such as nuts) exposed to high dry temperatures can be potent sources of these pro-oxidant chemicals.

In another study, researchers fed diabetics glycotoxin-packed foods, like chicken, fish, and eggs, and their inflammatory markers––tumor necrosis factor, C-reactive protein, and vascular adhesion molecules––shot up. “Thus, in diabetes, environmental (dietary) AGEs promote inflammatory mediators, leading to tissue injury.” The good news is that restriction of these kinds of foods may suppress these inflammatory effects. Appropriate measures to limit AGE intake, such as eliminating meat or using only steaming and boiling as methods for cooking it, “may greatly reduce the already heavy burden of these toxins in the diabetic patient.” These glycotoxins may be the missing link between the increased consumption of animal fat and meats and the development of type 2 diabetes.

Since the 2013 meta-analysis was published, another study came out in which approximately 17,000 people were followed for about a dozen years. Researchers found an 8% increased risk for every 50 grams of daily meat consumption. Just one quarter of a chicken breast’s worth of meat for the entire day may significantly increase the risk of diabetes. Yes, we know there are many possible culprits: the glycotoxins or trans fat in meat, saturated fat, or the heme iron (which could actually promote the formation of carcinogens called nitrosamines, though they could also just be produced in the cooking process itself). However, we did learn something new: There also appears to be a greater incidence of diabetes among those who handle meat for a living. Maybe there are some diabetes-causing zoonotic infectious agents––such as viruses––present in fresh cuts of meat, including poultry.

A “crucial factor underlying the diabetes epidemic” may be the overstimulation of the aging enzyme TOR pathway by excess food consumption––but not by the consumption of just any food: Animal proteins not only stimulate the cancer-promoting hormone insulin growth factor-1 but also provide high amounts of leucine, which stimulates TOR activation and appears to contribute to the burning out of the insulin-producing beta cells in the pancreas, contributing to type 2 diabetes. So, it’s not just the high fat and added sugars that are implicated; critical attention must be paid to the daily intake of animal proteins as well.

According to a study, “[i]n general, lower leucine levels are only reached by restriction of animal proteins.” To reach the leucine intake provided by dairy or meat, we’d have to eat 9 pounds of cabbage or 100 apples to take an extreme example. That just exemplifies the extreme differences in leucine amounts provided by a more standard diet in comparison with a more plant-based diet.

I reviewed the role endocrine-disrupting industrial pollutants in the food supply may play in a three-part video series: Fish and Diabetes, Diabetes and Dioxins, and Pollutants in Salmon and Our Own Fat. Clearly, the standard America diet and lifestyle contribute to the epidemic of diabetes and obesity, but the contribution of these industrial pollutants can no longer be ignored. We now have experimental evidence that exposure to industrial toxins alone induces weight gain and insulin resistance, and, therefore, may be an underappreciated cause of obesity and diabetes. Consider what’s happening to our infants: Obesity in a six-month-old is obviously not related to diet or lack of exercise. They’re now exposed to hundreds of chemicals from their moms, straight through the umbilical cord, some of which may be obesogenic (that is, obesity-generating).

The millions of pounds of chemicals and heavy metals released every year into our environment should make us all stop and think about how we live and the choices we make every day in the foods we eat. A 2014 review of the evidence on pollutants and diabetes noted that we can be exposed through toxic spills, but “most of the human exposure nowadays is from the ingestion of contaminated food as a result of bioaccumulation up the food chain. The main source (around 95%) of [persistent pollutant] intake is through dietary intake of animal fats.”


For more on the information mentioned here, see the following videos that take a closer look at these major topics:  

AGEs: Glycotoxins, Avoiding a Sugary Grave, and Reducing Glycotoxin Intake to Prevent Alzheimer’s.

TOR: Why Do We Age?, Caloric Restriction vs. Animal Protein Restriction, Prevent Cancer From Going on TOR, and Saving Lives By Treating Acne With Diet

Viruses: Infectobesity: Adenovirus 36 and Childhood Obesity

Poultry workers: Poultry Exposure and Neurological Disease, Poultry Exposure Tied to Liver and Pancreatic Cancer, and Eating Outside Our Kingdom

Industrial pollutants: Obesity-Causing Pollutants in Food, Fish and Diabetes, Diabetes and Dioxins, and Pollutants in Salmon and Our Own Fat

The link between meat and diabetes may also be due to a lack of sufficient protective components of plants in the diet, which is discussed in my videos How May Plants Protect Against Diabetes?, Plant-Based Diets for DiabetesPlant-Based Diets and Diabetes, and How Not to Die from Diabetes.

In health,

Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations: