Oxalate is a compound found in some foods, and it is also produced as a waste product by the body. It exits the body through the urine. Too much oxalate may cause kidney stones in some people.
Foods high in oxalate include:
Women have it so easy don’t they? Forget high heels and more expensive dry cleaning bills. Those are mild compared to menarche, menopause, and about forty years of menstruation in between. Under the best of circumstances, the hormonal fluctuations that accompany these events can make life “interesting” for the women experiencing them as well as for the men who are close to them. (Not to mention their kids and coworkers!) But throw in the curveballs of modern life—poor diet, inadequate sleep, relentless psychological stress, and an environment rife with inescapable estrogenic compounds in manmade goods—and the effects on a woman’s hormones make towering amusement park roller coasters look like the kiddie teacup ride.
The modern functional medicine practitioner is likely to encounter female patients presenting with issues resulting from excess estrogen, inadequate progesterone, or both. Such imbalances may occur in women of reproductive age as well as post-menopausal women, and they can have a significant negative impact on quality of life. Among women of reproductive age, signs and symptoms of excess estrogen relative to progesterone include decreased sex drive, irregular or abnormal periods (including excessive bleeding), bloating, breast swelling and tenderness, mood swings (especially irritability and depression), weight gain, cold hands and feet, and premenstrual headaches.
While compounds such as calcium-d-glucarate and di-indolylmethane (DIM) are effective for reducing estrogen levels, other interventions may be needed to boost flagging progesterone levels. Younger women may benefit from exogenous progesterone for the treatment of dysfunctional uterine bleeding resulting from anovulatory cycles, and progesterone may also be beneficial for endometrial hyperplasia due to chronic unopposed estrogen.
Adequate progesterone (“pro-gestation”) is essential for a healthy full-term pregnancy, so pregnant women and those who are trying to conceive should ensure sufficient levels. In patients with a history of unexplained recurrent miscarriages, progesterone supplementation has been shown to slightly reduce the rate of subsequent miscarriages. Progesterone administration may also reduce the risk for preterm delivery and perinatal mortality among women with previous preterm deliveries. (In vitro data show progesterone inhibits fetal membrane weakening.)
Data are mixed when it comes to progesterone boosting fertility among women being treated with agents to stimulate fertility and/or undergoing intrauterine insemination (IUI). On the whole, there does seem to be a role for progesterone in increasing the likelihood of conception. A systematic review and meta-analysis found that luteal phase progesterone supplementation significantly increases live birth among women undergoing IUI when receiving gonadotropins for ovulation induction, but not among women receiving clomiphene citrate (CC). However, another study determined that progesterone does aid in conception in women taking CC compared to those not treated with progesterone. But yet another study showed that luteal phase progesterone administration significantly increased conception rate among women with PCOS who were treated with letrozole, but not with CC.
As for post-menopausal women, the natural decrease in progesterone levels that occurs with aging may result in hot flashes, mood swings, urinary incontinence, hair loss, vaginal dryness, poor concentration, uterine fibroids, loss of libido and an overall decline in health and quality of life. Additional symptoms include trouble sleeping, brain fog, and others that overlap with symptoms in younger women: breast tenderness, mood swings, water retention, and weight gain. Fortunately, many of these unpleasant and in some cases debilitating symptoms may be improved through restoration of healthy progesterone levels.
Data suggest that mean serum progesterone (and estradiol) concentrations are significantly lower among menopausal women reporting hot flashes compared to those not reporting hot flashes, and that higher levels of these hormones are associated with decreased odds of hot flashes. Micronized progesterone supplementation has been shown to significantly decrease moderate to severe vasomotor symptoms compared to placebo in early postmenopausal women, and it doesn’t cause a rebound increase in occurrence when treatment is stopped.
As with estrogen, there are both synthetic and natural bioidentical progesterone formulations available. Synthetic preparations often induce significant side effects, such as fatigue, fluid retention, lipid level alterations, dysphoria, hypercoagulant states, and increased androgenicity. Natural progesterone may present fewer side-effects while being equally if not more bioavailable than synthetic forms. Natural progesterone is obtained primarily from plants and can be administered via injection, through intravaginal or oral formulations, or applied topically and absorbed through the skin. Patients being treated with exogenous hormones should be monitored closely to ensure healthy hormone levels.
Google Dr.Malcom Kendrick–he offers an enormous format of information on Statin Drugs
Story at-a-glance
Researchers have repeatedly failed to find evidence that high cholesterol is a risk factor for cardiovascular disease. In fact, there’s plenty of evidence suggesting that higher cholesterol may actually be healthier than lower levels.
As I’ve discussed in many previous articles, three (to some degree interrelated) factors that have a far greater influence on your cardiovascular disease (CVD) risk are:
Elevated iron levels will significantly contribute to inflammation, but even if your iron is normal, chronic inflammation can be caused by a wide range of factors, starting with your diet. Your diet is also the key factor at play when it comes to your insulin level, and can worsen the effects of iron overload.
Unfortunately, these primary contributors are rarely the focus of CVD prevention and treatment in conventional medicine. Instead, statins (cholesterol lowering drugs) are the go-to first line of defense, and this despite the many studies showing cholesterol isn’t a part of the problem.
Eye-Opening Finding: Statins Extend Life by About Three Days
A systematic review4 published in 2015 that deserves far more attention than it has received assessed the ability of statins to postpone death and improve mortality rates. Eleven statin trials with a follow-up between two and 6.1 years were included in the review.
In primary prevention trials (meaning studies in which statins were used as a primary prevention for CVD), death was postponed between a negative five days (meaning they died five days sooner than the control group) and 19 days.
In secondary prevention trials, death was postponed between a negative 10 days and 27 days. The median postponement of death in primary prevention trials was 3.2 days, and in secondary prevention trials 4.1 days.
This is a truly astounding finding, considering people take stains for years, if not decades, and the fact that these drugs are associated with a wide range of serious side effects that can decimate quality of life.
British MP Calls for Parliamentary Inquiry Into Statins
The good news is, more and more scientists are now starting to see this truth. A March 9, 2019, article5 in European Scientist reported:
“Earlier this week, the Chair of the British Parliament Science and Technology Committee, Sir Norman Lamb MP made calls for a full investigation into cholesterol lowering statin drugs.
It was instigated after a letter was written to him signed by a number of eminent international doctors including the editor of the BMJ, the Past President of the Royal College of Physicians and the Director of the Centre of Evidence Based Medicine in Brazil … calling for a full parliamentary inquiry into the controversial medication.”
In the article, the lead author of the letter, cardiologist Aseem Malhotra, discusses the dangers of statins, and how the flawed cholesterol hypothesis and the corresponding low-fat myth are pushing patients’ health in the wrong direction. He writes, in part:6
“It is not just financial interests that bias research findings but also intellectual hubris in medicine too. It was the father of the evidence based medicine movement the late Professor David Sackett who said ‘Fifty percent of what you learn in medical school will turn out to be either outdated or dead wrong within five years of your graduation, the trouble is no one can tell you which half so you have to learn to learn on your own.’
In the past 30 years, there have now been 44 randomized controlled trials that reveal no cardiovascular mortality benefit from diet or various drug trials from lowering cholesterol.
Most conspicuous was the recent ACCELERATE trial with over 12,000 patients at high risk of heart disease that revealed no reductions in heart attack, stroke or death despite a 37% reduction in LDL-cholesterol.
But how many doctors actually keep up with the latest evidence? Many will defend the cholesterol lowering dogma with their more inquisitive patients by saying they’re just following guidelines, unaware that the guidelines themselves are based upon biased research often written by scientists with strong personal or institutional financial ties to the industry.”
Scientific Review Declares Statin Claims Are Overblow
Another newsworthy review7 that ties into Malhotra’s arguments against statins was published in the Expert Review of Clinical Pharmacology in September 2018. It identified significant flaws in three recent studies “published by statin advocates” attempting “to validate the current dogma.”
The paper presents substantial evidence that total cholesterol and low-density lipoprotein (LDL) cholesterol levels are not an indication of heart disease risk, and that statin treatment is of “doubtful benefit” as a form of primary prevention for this reason. The paper also details the tactics used in statin studies to exaggerate the benefits. Among them:
• Excluding unsuccessful trials where statins either had no or negative impact on CVD risk or mortality
• Using “evidence” that isn’t a true exposure-response
• Cherry-picking data that supports the conclusion of benefit
• Ignoring the most important outcome — an increase in life expectancy
• Using a statistical tool called relative risk reduction to amplify trivial effects — This was also addressed more directly in a 2015 report8,9 titled “How Statistical Deception Created the Appearance That Statins Are Safe and Effective in Primary and Secondary Prevention of Cardiovascular Disease.”
Here, the authors point out that if you look at absolute risk, statin drugs benefit just “1% of the treated participants.”10 This means that out of 100 people treated with the drugs for five years, one person will have one less heart attack.
According to the authors of the 2018 review:11
“For some years, many researchers have questioned the results from statin trials because they have been denied access to the primary data. In 2004–2005, health authorities in Europe and the United States introduced New Clinical Trial Regulations, which specified that all trial data had to be made public. Since 2005, claims of benefit from statin trials have virtually disappeared.”
How Statin Studies Minimize Appearance of Side Effects
The Expert Review of Clinical Pharmacology paper also points out that statin trials minimize health risks by using a run-in period. Essentially, the participants are given the drug for a few weeks, after which those who suffer adverse effects are simply excluded.12 Needless to say, this automatically lowers the number of perceived side effects.
In reality, serious side effects may affect anywhere from 20% to 50% of statin users.13 What’s more, muscle damage is likely far more common a side effect than most statin studies claim.
The authors cite one study in which myopathy occurred in just 0.01% of treated individuals. However, myopathy was defined as having a creatine kinase level “more than 10 times higher than normal,” the authors note.14
Meanwhile, other research that looked at muscle biopsies found patients with normal creatine kinase levels, who complained of muscular symptoms, indeed had microscopic signs of myopathy. “When patients stopped treatment, their symptoms disappeared, and repeated biopsies showed resolution of the pathological changes,” the authors note, adding that:15
“To reject the frequent occurrence of muscular problems with the argument that muscle symptoms are nocebo effects is also invalid. In a study of 22 statin-treated professional athletes, the authors reported that 17 (77%) of the athletes terminated treatment because of muscular symptoms, which disappeared a few days or weeks after drug withdrawal.
The explanation for statin-induced adverse muscle effects is probably that statin treatment not only blocks the production of cholesterol but also blocks the production of several other important molecules, for instance, coenzyme Q10, which is indispensable for energy production.
As most energy is produced in the muscle cells, including those of the heart, the extensive use of statin treatment may explain the epidemics of heart failure that have been observed in many countries.”
Another study16 published in 2011 supports these statements, concluding that statin treatment lasting longer than two years causes “definite damage to peripheral nerves.”
A study17 published in the August 2019 issue of JACC: Basic to Translational Science presents a new mechanism of statin-induced myopathy. In short, the data suggest statin treatment causes calcium to leak out of your muscle cells.
As explained by Science Daily,18 “Under normal conditions, coordinated releases of calcium from these stores make the muscles contract. Unregulated calcium leaks may cause damage to muscle cells, potentially leading to muscle pain and weakness.”
Statin Use Is Associated With a Wide Variety of Problems
In their Expert Review of Clinical Pharmacology paper, the authors also highlight research showing statin use is associated with a number of significant health complications beside muscle problems:19
“… [C]ase–control and cross-sectional studies have shown that statin use is observed significantly more often among patients with cataracts, hearing loss, suicidal ideation, peripheral neuropathy, depression, Parkinson’s disease, interstitial cystitis, herpes zoster, impotency, cognitive impairments, and diabetes.
In some of these studies, the side effects disappeared with discontinuation of the statins and worsened with rechallenge. As cholesterol is a vital substance for the renewal of all cells, and since statins also block the production of other molecules necessary for normal cell function, it is not surprising that statin treatment may result in side effects from many different organs.”
Even More Reasons to Avoid Statin Drugs
The scientific fact is, aside from being a “waste of time” and not doing anything to reduce mortality, statins also come with a long list of potential side effects and clinical challenges. Importantly, statins:
1. Deplete your body of CoQ10 — Statins block HMG coenzyme A reductase in your liver, which is how they reduce cholesterol. But this is also the same enzyme that makes CoQ10, which is an essential mitochondrial nutrient that facilitates ATP production.
2. Inhibit the synthesis of vitamin K2, a vitamin that protects your arteries from calcification.
3. Because of 2 and 3, statins increase your risk for other serious diseases. Aside from the conditions mentioned above, they may also raise your risk for:
a. Cancer — Research20 has shown that long-term statin use (10 years or longer) more than doubles women’s risk of two major types of breast cancer: invasive ductal carcinoma and invasive lobular carcinoma.
b. Diabetes — Statins have been shown to increase your risk of diabetes via a number of different mechanisms, two of which include increasing your insulin resistance, and raising your blood sugar. According to one recent study,21 statins double your risk of Type 2 diabetes, and triple the risk when taken for more than two years.
c. Cognitive dysfunction, neurological damage22 and neurodegenerative diseases, including vascular dementia, Alzheimer’s disease and Parkinson’s disease.23
d. Decreased heart function.24
e. Impaired fertility — Importantly, statins are a Category X medication,25 meaning they cause serious birth defects,26 so they should never be used by a pregnant woman or women planning a pregnancy.
Statins Do Not Benefit Patients With Respiratory Disease
Aside from lowering cholesterol, statins appear to have an ameliorating effect on inflammation. For this reason, statins are at times used in the treatment of pulmonary conditions such as chronic obstructive pulmonary disease (COPD). This may be because statins are a Nrf2 activator27 and decrease oxidative stress and secondary inflammation.
However, while some observational studies have shown a potential benefit, a July 2019 systematic review28 by the Cochrane Database of Systematic Reviews failed to find any significant benefit for this patient group. The review had three primary objectives:
a. To determine whether statins reduce mortality rates in COPD
b. To determine whether statins reduce exacerbation frequency, improve quality of life, or improve lung function in COPD
c. To determine whether statins are associated with adverse effects
The review included eight placebo-controlled studies involving 1,323 participants with COPD, with a mean age of 61.4 to 72 years. According to the authors:29
“We found no statistically significant difference between statins and placebo in our primary outcome of number of exacerbations per person‐year, including number of exacerbations requiring hospitalization per person‐year …
Our primary outcomes of all‐cause mortality and COPD‐specific mortality showed no significant difference between statins and placebo, with wide confidence intervals suggesting uncertainty about the precision of the results … Results show no clear difference in quality of life, which was reported in three trials …
A small number of trials providing low‐ or moderate‐quality evidence were suitable for inclusion in this review. They showed that use of statins resulted in a reduction in CRP and IL‐6, but that this did not translate into clear clinical benefit for people with COPD.”
Beware: Next-Gen Cholesterol Drugs Likely Just as Harmful
While some of the dangers of statins are becoming more widely recognized, the dangers of cholesterol-lowering drugs in general is still being swept under the rug as newer drugs are being released.
One next-gen class of cholesterol-lowering drugs is the proprotein convertase substilisin/kexin type 9 (PSCK9) category, also known as PCSK9 Inhibitors.30 Just as there are many different drugs within the statin category, there are many in the PSCK9 category. Repatha is one of them.
PCSK9 is a protein that works with LDL receptors that regulate LDL in your liver and release LDL cholesterol into your blood. The inhibitors work by blocking that protein, thus lowering the LDL in circulation.
While these drugs are being touted as the answer for those who cannot tolerate some of the side effects of statins, such as severe muscle pain, there’s already evidence suggesting PCSK9 inhibitors can produce neurocognitive effects, with some patients experiencing confusion and attention deficits.31,32,33,34
At the end of the day, if you’re concerned about your heart health, you’d be wise to implement lifestyle changes known to support a healthy heart and help prevent CVD from developing in the first place. You can learn more about your risk factors, recommended tests and drug-free prevention methods in the following articles: “Cholesterol Does Not Cause Heart Disease,” “How to Increase Your Health Span,” and “Why Your Doctor Is Wrong About Cholesterol.”
Rosacea is an inflammatory skin disease with an elusive pathology that is thought to include a combination of microorganisms, genetic predisposition, abnormal neurological signaling, a disrupted innate immune system, and dysbiosis. The clinical presentations can differ slightly between individuals and help classify rosacea into one of four subtypes: erythematotelangiectatic, papulopustular, phymatous, and ocular.
Traditional therapy has focused on anti-inflammatory antibiotics, but long-term pharmaceutical therapy is rarely a desirable option due to the risk of gastrointestinal distress and antibiotic resistance. It is also well known that there are specific triggers that exacerbate rosacea including heat, sun exposure, spicy foods, alcohol consumption, exercise, and heightened emotions. Given the fact that none of these are modulated by antibiotics, questions are raised regarding other treatment modalities that may more effectively address the underlying causes of rosacea. Diet is increasingly becoming the focus as we learn more about the gut-skin axis and its influence upon many of the elements of rosacea including the microbial, inflammatory, and immune components.
Diet is unquestioningly becoming an aspect of managing all subtypes of rosacea. According to a survey by the National Rosacea Society, 78 percent of the 400+ patients surveyed had altered their diet due to rosacea; and of this group, 95 percent reported a reduction in flares. Of the dietary triggers reported in this survey, most fell into 4 groups: heat-related (hot coffee, tea), alcohol-related (wine, hard liquor), capsaicin-related (spices, pepper, hot sauces), and cinnamaldehyde-related (tomatoes, citrus, cinnamon, chocolate). One explanation for the triggering effects of these foods is their ability to stimulate vanilloid channels which are active in patients with rosacea. When these channels are activated, they increase blood flow to the skin via neurogenic vasodilatation, which causes the flushing and burning associated with this condition.
In a multicenter retrospective case-control survey of 2637 subjects (controls and patients with rosacea) that sought to find a relationship between diet and rosacea, a high-frequency intake of fatty food and tea was associated with rosacea, while a high-frequency of dairy products negatively correlated with it (and may have actually been linked to a reduction in rosacea severity).
The gut-skin axis is another explanation for the link between diet and rosacea. Anecdotally, many patients with rosacea also experience gastrointestinal conditions. A population-based cohort study of nearly 50,000 Danish patients with rosacea discovered a high prevalence of celiac disease, Crohn’s disease, ulcerative colitis, Helicobacter pylori infection, small intestinal bacterial overgrowth (SIBO), and irritable bowel syndrome. Research has already confirmed a direct link between the microbiome of the gut and the robustness of the immune system. Additionally, since the body’s inflammatory response is a role of the immune system, these cannot be treated separately. Therefore, it should be no surprise that rosacea – a condition with immunological and inflammatory-based pathology – is also associated with gastrointestinal conditions that are rooted in an unhealthy microbiome. This association is further strengthened by the fact that antibiotics often lead to short-term improvement but are not a long-term solution. Initially, antibiotics eradicate the pathogenic organisms from the gut, but without adequate probiotic and dietary support to rebuild a healthy microbiome, the positive effect of the antibiotics diminishes and eventually has an opposing effect on the gut.
The microbiome of the gut has also been shown to influence the microbial composition of the skin, which may affect the bacterial component of rosacea. Further, the skin microbiome modulates the immune response at the surface of the skin. Since the pathology of rosacea involves a dysregulated innate immune response, including enhanced expression of toll-like receptor 2 in the epidermis of rosacea patients, correcting the gut microbiome may be a foundational process for rebalancing the microorganisms and immune response of the skin.
Dietary patterns that support a balanced microbiome include 1) fermented, probiotic-rich foods such as yogurt, kefir, miso, kimchi, and sauerkraut; 2) dietary plant fiber to serve as prebiotics; and 3) cold-water fish and seafood, and/or omega-3 fatty acid supplements as substrates for anti-inflammatory prostaglandins that competitively inhibit pro-inflammatory pathways. Low-carb, high-protein diets, such as a Paleolithic diet, have been shown to positively modulate the microbiome since they eliminate sugar sources that foster the growth of pathogenic bacteria while providing nutrients that modulate the inflammatory response and promote a favorable environment for beneficial organisms.
Individuals suffering from rosacea often groan as the summer months progress since the heat and sun often exacerbate the flare-ups; however, rosacea is far less of a seasonal problem and more of a year-round gastrointestinal problem, meaning its management needs to begin with a closer look at the diet.
Here are a list of Iodine links that I feel you should read and save in your Dr. Princetta file.
My position on breast cancer is to take matters into your own hands so as to prevent breast cancer at all cost.
In a nutshell, Iodine decreases the ability of estrogen to adhere to estrogen receptors in the breast
Theoretically we all should get our nutrients from food. Seaweeds have the highest Iodine content but unlike the Japanese, American do not eat seaweeds such as Nori, Wakame, Kombu or Dulse. I am attaching a list of foods high in Iodine to this e-mail
Because you cannot depend on diet alone to provide Iodine, I recommend the best products available such as:
1. Edgar Cayce Detoxified Iodine: 2-4 drops in water once or twice daily
2. Iodoral 12.5 mg: 1 per day x 3 weeks then 1 tab 3x weekly–decreasing gradually
3. Dr. Carolyn Dean’s Re-Myte (12 minerals; 9 of which are thyroid specific)
Here are the links I think you should take a look at:
From a testing perspective, I recommend the following:
Who Should be Tested for BRCA Mutations?
NOTE: Because of estrogen, breast and ovarian cancers run in the same circle!
Please forward this information to everyone you know.
Clostridium difficile loves sugar and resists disinfectant
Story at-a-glance
The Centers for Disease Control and Prevention1 calls antibiotic resistance one of the biggest public health challenges of our time. Conservative estimates find at least 2 million are infected and 23,000 die each year with antibiotic resistant bacteria. When a germ develops the ability to withstand drugs designed to kill them, they become antibiotic-resistant2 and are called superbugs.3
Antibiotic resistance happens naturally as bacteria adapt to drugs. Resistance is helped along by the inappropriate use of medications, such as antibiotics for viral infections4 and their use in agriculture.5,6 The World Health Organization7 warns emerging resistance to antibiotics threatens the ability to treat common infections that may result in prolonged illness, disability and death.
Simple medical procedures may become high risk, which means the cost of health care rises. In what researchers believed was the first national estimate8 of the cost for treating antibiotic-resistant infections, they found a national cost of $2.2 billion in 2014, having doubled since 2002.9
Antibiotic resistance is a worldwide crisis10 with the potential to threaten people at any age.11 One bacterium known to be fatal to the elderly and sick is clostridium difficile, or C. diff. In a recent study it was reported that this12 bacterium has become highly adapted to spreading inside hospitals, and they may have found the reason why.
Bacteria and sugar make a deadly combination
A mild to moderate infection with this bacterium affects the gut, causing watery diarrhea for two to three days and mild abdominal cramping and tenderness.13 A severe infection can trigger diarrhea, fever, kidney failure, dehydration and weight loss.14
The bacteria are now able to take advantage of high sugar diets and resist disinfection commonly used in the hospital. In a recent study15 researchers showed how C. diff can exist for long periods of time on disposable equipment and vinyl surfaces, even after having been cleaned with disinfectant.
In one study published in Nature16 it was reported that C. diff has adapted and diverged, and is close to becoming a new bacterial species. Through a large-scale analysis of 906 cultures taken from humans, animals and the environment17 the researchers sequenced the bacterium’s DNA and were able to demonstrate the evolving formation of a new species18 with a change in metabolism and sporulation.19
The new evolution of C. diff is producing spores more resistant to hospital disinfectants that have the capacity to grow in the presence of glucose and fructose. The researchers found the new species in 70% of hospital patient samples taken for the study.
They also found this new species could colonize mice better when the animals’ diet was supplemented with sugar. Analysis found this emerging species made its first appearance 76,000 years ago and has more recently begun to thrive in hospital settings. Senior author Trevor Lawley commented:20
“Our study provides genome and laboratory-based evidence that human lifestyles can drive bacteria to form new species so they can spread more effectively. We show that strains of C. difficile bacteria have continued to evolve in response to modern diets and healthcare systems and reveal that focusing on diet and looking for new disinfectants could help in the fight against this bacteria.”
C. diff is commonly found in the environment
Another author of the paper, Nitin Kumar, Ph.D., a senior bioinformatician at the Wellcome Sanger Institute, told Popular Science:21 “The study shows how the pathogen C. difficile is evolving in response to the Western sugary diet and common hospital disinfectants.”
A New York Post journalist suggests pudding cups and instant mashed potatoes, common fare at hospitals, may be just the food this superbug is looking for.22 According to Harvard Health, C. diff accounts for up to 3% of bacteria in a normal intestinal flora. Although present, it is usually harmless as good bacteria keep it under control.
It turns out that antibiotics have turned this minor player into a major problem.23 Once antibiotics have disrupted the normal flora in your gut, this allows harmful bacteria to thrive, including C. diff. This in turn triggers diarrhea.24
C. diff forms spores that may get into the environment through those who are infected, when they touch surfaces. When others touch the newly-contaminated surfaces and then touch their mouths, the infection spreads.25
Health care workers may also spread the bacteria when their hands are contaminated. Since antibiotics alter the normal flora found in the intestinal tract, and a large number of patients receive antibiotics in health care settings, this can lead to C. diff outbreaks.
Poop pills may help combat an outbreak
C. diff can trigger a life-threatening condition in those who have been on antibiotics or have a compromised immune system. According to the CDC, there are 500,000 C. diff infections each year resulting in 15,000 deaths.26 One treatment methodology is a stool transplant, which has been used throughout history.
Although new to Western medicine, fecal transplants were described as far back as 1,700 years ago by a Chinese researcher who first used what he called “yellow soup” to treat patients with severe diarrhea.27 In World War II, the stools of camels was used to treat bacterial dysentery in German soldiers.
In 1958, the treatment was described in a report for a patient with antibiotic-associated diarrhea. But it was not until 1978 that the value was recognized in the treatment of C. diff.28 The treatment goes under several different names including fecal biotherapy and fecal floral reconstitution.
In the past, colonoscopies have been the most successful way of introducing fecal matter into patients, but a new poop pill-popping protocol may be less invasive while still offering a life-saving option. In a trial at the University of Alberta,29 researchers compared the administration of fecal matter using a capsule or colonoscopy.
All participants in the study had suffered a minimum of three bouts of C. diff. Both groups showed prevention of recurrent infection in 96.2% of the participants.30 While the colonoscopy was invasive, the patient chosen to swallow pills had to down 40 capsules in one sitting.31
Using poop pills is noninvasive, less expensive, free of risks associated with sedation and may be done in the doctor’s office. It is not, however, a treatment method you should experiment with at home. Even under investigational conditions, mistakes can be made.
In June 2019, the FDA released a statement that two immunocompromised adults had received a transplant that unwittingly transmitted a multidrug-resistant organism. At least one of those patients has died.32
Prevention is still the best medicine
To date, the FDA has not approved fecal transplants and continues to monitor the development as it is essential for a healthy donor to be used.33 Open Biome maintains a list of current studies being done on fecal transplants including those to treat C. diff, inflammatory bowel disease, liver disease, obesity and depression.34
The single most effective means to prevent the spread of infection is through hand washing. The CDC35 recommends cleaning your hands to prevent the spread of germs. However, they find on average health care workers do this less than half the time they should.
In one cross-sectional study36 conducted in Nepal to assess the habits of nurses, nursing students, doctors and medical students, the researchers found a significant difference in hand washing both before and after patient care.
After exposure to instruments, blood or bodily fluid, more than 90% washed their hands. However, on average the participants tended to wash their hands selectively.
A second study of hand washing in six intensive care units revealed a high level of variability in adherence to best practices with a compliance rate ranging from 3% to 100%.37 Take care to use proper handwashing techniques to thoroughly clean your hands and reduce the risk of transmitting disease.
A second preventive strategy includes protecting your gut microbiome from the effects of antibiotics. It is important to take antibiotics only when they’re necessary. You should not use them for viral infections, which may contribute to the development of antibiotic resistance.38
Antibiotics have no effect on viruses and you’ll likely get greater relief by using a combination of natural remedies described in my previous article, “Natural Cold Remedies: What Works, What Doesn’t.”
Support strong gut bacteria for good health
Supporting the growth of beneficial bacteria in your gut microbiome may affect your mental and physical health. Sugar is one of the most negative culprits because it contributes to a dysfunctional gut microbiome. A study39 published in January 2019, found that sugars affect a regulator of gut colonization for beneficial bacteria.
In essence, glucose and fructose turn off the expression of a protein regulating gut colonization by beneficial microbes. Sugar disrupts the generation of proteins that foster the growth of beneficial bacteria found in lean, healthy individuals.40
Since gut dysfunction may lead to a system-wide inflammatory response, it is important to address the needs of your gut bacteria consistently. As a general rule, once you start healing your gut, you should start feeling better in a couple of weeks to a few months. Discover several strategies to help you get started in my article, “Healthy Gut, Healthy You: A Personalized Plan to Transform Your Health.”
By Anne Underwood On 7/4/99 at 8:00 PM EDT Share News
She was making lunch for herself and a friend one Saturday this spring when an unfamiliar feeling swept over her. The 50-year-old social worker had fallen deep into depression two years earlier, and had given up on prescription antidepressants when the first one she tried left her sluggish, sexually dormant and numb to her own emotions. Then, in mid-March, she heard about a naturally occurring substance called SAMe (pronounced “Sammy”). She had been taking it for just a few days when she began setting the table that Saturday morning. A ginger-miso sauce was chilling in the fridge, and she was garnishing her finest plates with fresh anemones. Suddenly, there it was: a sense of undiluted pleasure.
This woman (who asked not to be named) has taken SAMe ever since, and her mood isn’t the only thing that has changed. Until this spring she took prescription-strength anti-inflammatories for her arthritis, and still had trouble bending her knees. She’s now off those drugs–and feeling more nimble than she has in 20 years.
Could an over-the-counter tonic really do all this? Pills purporting to cure everything from hemorrhoids to hangnails are usually worthless and sometimes dangerous. And because SAMe has not been studied extensively in the United States, many doctors are leery. Beware, says Dr. Gilbert Ross of the American Council on Science and Health, a conservative watchdog group. Supplement dealers are once again trying to “flimflam the public into using untested remedies instead of FDA-approved pharmaceuticals.”
The Food and Drug Administration has not rigorously evaluated SAMe, let alone approved it. (Federal law permits the unregulated sale of naturally occurring substances as long as marketers avoid therapeutic claims.) And the studies that researchers have conducted are not of the magnitude the FDA would require for a drug approval. But that doesn’t mean SAMe is “untested.” In dozens of European trials involving thousands of patients, it has performed as well as traditional treatments for arthritis and major depression. Research suggests it can also ease normally intractable liver conditions. SAMe doesn’t seem to cause adverse effects, even at high doses. And doctors have prescribed it successfully for two decades in the 14 countries where it has been approved as a drug.
Until recently, few Americans had heard of the stuff. An Italian firm developed it as a pharmaceutical in the early 1970s but lacked the will or the resources to make a run at a drug approval in the United States. Then, this spring, two U.S. vitamin companies, GNC and Pharmavite, started importing large quantities of SAMe to sell as a supplement. The product took off quickly–Pharmavite’s Nature Made brand now ranks 25th among the 13,000 supplements sold in grocery and drugstores–and the impact is still growing. When you consider that some 50 million Americans suffer from arthritis or depression, the implications are staggering.
SAMe (known formally as S-adenosylmethionine) is not an herb or a hormone. It’s a molecule that all living cells, including our own, produce constantly. To appreciate its importance, you need to understand a process called methylation (chart). It’s a simple transaction in which one molecule donates a four-atom appendage–a so-called methyl group–to a neighboring molecule. Both the donor and the recipient change shape in the process, and the transformations can have far-reaching effects. Methylation occurs a billion times a second throughout the body, affecting everything from fetal development to brain function. It regulates the expression of genes. It preserves the fatty membranes that insulate our cells. And it helps regulate the action of various hormones and neurotransmitters, including serotonin, melatonin, dopamine and adrenaline. As biochemist Craig Cooney observes in his new book, “Methyl Magic,” “Without methylation there could be no life as we know it.”
And without SAMe, there could be no methylation as we know it. Though various molecules can pass methyl groups to their neighbors, SAMe is the most active of all methyl donors. Our bodies make SAMe from methionine, an amino acid found in protein-rich foods, then continually recycle it. Once a SAMe molecule loses its methyl group, it breaks down to form homocysteine. Homocysteine is extremely toxic if it builds up within cells. But with the help of several B vitamins (B6, B12 and folic acid), our bodies convert homocysteine into glutathione, a valuable antioxidant, or “remethylate” it back into methionine.
SAMe and homocysteine are essentially two versions of the same molecule–one benign and one dangerous. When our cells are well stocked with B vitamins, the brisk pace of methylation keeps homocysteine levels low. But when we’re low on those vitamins, homocysteine can build up quickly, stalling the production of SAMe and causing countless health problems. High homocysteine is a major risk factor for heart attack and stroke. During pregnancy, it raises the risk of spina bifida and other birth defects. And many studies have implicated it in depression.
How, exactly, might taking extra SAMe improve a person’s mood? Researchers have identified several possibilities. Normal brain function involves the passage of chemical messengers between cells. SAMe may enhance the impact of mood-boosting messengers such as serotonin and dopamine–either by regulating their breakdown or by speeding production of the receptor molecules they latch on to. SAMe may also make existing receptors more responsive. These molecules float in the outer membranes of brain cells like swimmers treading water in a pool. If the membranes get thick and glutinous, due to age or other assaults, the receptors lose their ability to move and change in response to chemical signals. By methylating fats called phospholipids, SAMe keeps the membranes fluid and the receptors mobile.
Whatever the mechanism, there is little question that SAMe can help fight depression. Since the 1970s, researchers have published 40 clinical studies involving roughly 1,400 patients. And though the studies are small by FDA standards, the findings are remarkably consistent. In 1994 Dr. Giorgio Bressa, a psychiatrist at the University Cattolica Sacro Cuore in Rome, pooled results from a dozen controlled trials and found that “the efficacy of SAMe in treating depressive syndromes… is superior [to] that of placebo and comparable to that of standard… antidepressants.”
This isn’t the first natural substance to show promise as a mood booster. Small studies suggest that St. John’s wort can ease low-grade melancholy, but SAMe has been tested against far more serious disorders. In one of several small U.S. studies, researchers at the University of California, Irvine, gave 17 severely depressed patients a four-week course of SAMe (1,600 mg daily) or desipramine, a well-established antidepressant. The SAMe recipients enjoyed a slightly higher response rate (62 percent) than the folks on desipramine (50 percent).
No one has found SAMe significantly more effective than a prescription antidepressant, but it’s clearly less toxic. The drugs that predate Prozac (tricyclics and MAO inhibitors) can be deadly in overdose, or in combination with other medications. Newer antidepressants, such as Prozac, Zoloft and Paxil, are less dangerous, but their known side effects range from headaches and diarrhea to agitation, sleeplessness and sexual dysfunction. And SAMe? Studies suggest that like other antidepressants, it may trigger manic episodes in people with bipolar disorder. Aside from that, the most serious side effect is a mild stomach upset.
Until large U.S. studies confirm these findings, few American doctors will recommend SAMe to severely depressed people. “The evidence looks promising,” says Harvard psychiatrist Maurizio Fava, “but it’s not definitive. In some European countries they have different marketing standards than we do.” UCLA biochemist Steven Clarke echoes that concern, saying the nation is embarking on a large, uncontrolled experiment in which consumers are the guinea pigs. A key concern is that depressed patients will drop other treatments to try SAMe, and end up suicidal. Columbia University psychiatrist Richard Brown warns of that hazard in “Stop Depression Now,” a new book coauthored with Baylor University neuropharmacologist Teodoro Bottiglieri. Yet Brown himself has treated several hundred patients with SAMe in recent years, sometimes combining it with other drugs, and he has never had a bad experience. “It’s the best antidepressant I’ve ever prescribed,” he says flatly. “I’ve seen only benefits.”
If the world needs a better antidepressant, it could also use a better arthritis remedy. Nearly a third of the 40 million Americans with chronic joint pain use drugs like aspirin and ibuprofen. In arthritis-strength doses, these so-called NSAIDs, or nonsteroidal anti-inflammatory drugs, can have devastating gastric side effects. Some 103,000 Americans are hospitalized annually for NSAID- induced ulcers, and 16,500 die. Even when NSAIDs don’t destroy the digestive tract, they may ultimately worsen people’s joint problems, for they slow the production of collagen and proteoglycans, the tissues that make cartilage an effective shock absorber.
Could SAMe provide an alternative? In a dozen clinical trials involving more than 22,000 patients, researchers have found SAMe as effective as pharmaceutical treatments for pain and inflammation. But unlike the NSAIDs, SAMe shows no sign of damaging the digestive tract. And instead of speeding the breakdown of cartilage, SAMe may help restore it. You’ll recall that after giving up its methyl group, SAMe becomes homocysteine, which can be broken down to form glutathione (the antioxidant) or remethylated to form methionine (the precursor to SAMe). As luck would have it, the reactions that produce glutathione also yield molecules called sulfate groups, which help generate those joint-sparing proteoglycans.
What does this mean for patients? The Arthritis Foundation, a mainstream advocacy group, recently said its medical experts were satisfied that SAMe “provides pain relief” but not that it “contributes to joint health.” The evidence that SAMe can repair cartilage is admittedly preliminary, but it’s intriguing. When German researchers gave 21 patients either SAMe or a placebo for three months, using MRI scans to monitor the cartilage in their hands, the SAMe recipients showed measurable improvements. That wouldn’t surprise Inge Kracke of Cologne. She was an active 48-year-old when a 1996 auto accident mangled her left knee and left her hobbling on a cane. Dr. Peter Billigmann of the University of Landau prescribed a regimen that combined SAMe (1,200 mg a day for three months) with injections of hyaluronic acid, a cartilage component. Cartilage injuries don’t normally heal, but a year later Kracke’s knee looked better on X-rays. She now plays golf three times a week.
SAMe may have other benefits as well. Studies suggest it can help normalize liver function in patients with cirrhosis, hepatitis and cholestasis (blockage of the bile ducts). SAMe has also been found to prevent or reverse liver damage caused by certain drugs. As patients hear more about this supplement, they may try treating themselves for all these conditions and others. But many of them will be disappointed–either because they expect miracles that SAMe can’t deliver, or because they take the wrong dose or form.
The first challenge is to buy full-strength SAMe. “Some companies are very reliable manufacturers,” says Dr. Paul Packman of Washington University in St. Louis. “But some aren’t. You can’t always tell from the label on the bottle how much active ingredient is actually in it.” Pharmaceutical-grade SAMe comes in two forms, one called tosylate and a newer, more stable form called butanedisulfonate. Only Nature Made and GNC sell the new butanedisulfonate version, but several U.S. retailers import reliable tosylate products. And because SAMe is absorbed mainly through the intestine, it’s best taken in “enteric coated” tablets that pass through the stomach intact. None of the products comes cheap. The price of a 400-mg dose ranges from $2.50 (Nature Made) up to $18.56 for an uncoated Natrol product called SAM sulfate. Promoted Content
Assuming you buy full-strength SAMe, the second challenge is to use it effectively. Experts advise taking it twice a day on an empty stomach, but different people may require different amounts. Though studies suggest that 400 mg a day is an effective dose for arthritis, the daily doses used in depression trials have ranged as high as 1,600 mg. Clinicians generally start people with mood problems at 400 and ratchet up as necessary.
Unfortunately, there is no convincing evidence that SAMe can make healthy people happier or more mobile than they already are. But there are lessons here for everyone. We now know that methylation is vital to our well-being. It’s equally clear that the modern Western diet–rich in protein, light on the plant foods that supply folate–is a prescription for stalling that vital process. “SAMe works as a medication to treat certain diseases,” says Paul Frankel, a biostatistician at the City of Hope National Medical Center in Duarte, Calif. “But for most people the problem is undermethylation of homocysteine.” In other words, many of us could arm ourselves against low moods, bad joints and weak hearts simply by upping our intake of B vitamins. That may sound less exciting than taking a miracle supplement. But with luck, it could keep you from ever needing one.