Best known for its natural antibiotic activity, berberine deals a serious blow to common infectious organisms—organisms like “staph,” “strep,” Chlamydia, diphtheria, salmonella, cholera, diplococcus pneumoniae, pseudomonas, gonorrhea, candida, trichomonas, and many others. Berberine is a component (for the technically inclined, a “plant alkaloid”) of the commonly used herbs goldenseal and Oregon grape, and of several other less well-known botanicals. A 0.2 percent solution of berberine has been found effective against trachoma—in “third world” countries, a major infectious cause of visual impairment and blindness, as well as many other types of conjunctivitis.
It’s less well known that berberine has been found more effective than aspirin in relieving fever in experimental animals, and is able to stimulate some parts of the immune system. It’s also a stimulant for bile secretion.
And it’s not at all well known that research published in well-known, respected, “peer-reviewed” medical journals in 2008 found that berberine is just as effective—and of course much safer—than metformin, the formerly patent medicine most commonly now prescribed to help re-regulate blood sugar in type 2 diabetes!
Another cover-up? That won’t stop the truthAs this is 2010, where has this information been? I suspect that Nutrition & Healing readers know the answer…so let’s move on to review the research, and then what’s known about how berberine does this job.
Two studies were reported in one of the 2008 research reports.1 In the first study, 36 adults with newly diagnosed type 2 diabetes mellitus were randomly assigned to treatment with berberine or metformin (500 milligrams of either, three times a day) in a three-month (13-week) trial.
At the end of three months, average fasting blood sugars in the berberine group dropped from 191 to 124 milligrams per deciliter, average post-prandial blood sugar (blood sugar after eating) dropped from 356 to 199 milligrams per deciliter, average hemoglobin A1c (a measurement of longer-term blood sugar control) dropped from 9.5 percent to 7.5 percent, and fasting triglycerides dropped from an average 99 to 78 milligrams per deciliter.
The researchers wrote, “Compared with metformin, berberine exhibited an identical effect in the regulation of glucose metabolism, such as HbA1c, FBG [fasting blood glucose], PBG [blood sugar after eating], fasting insulin and postprandial insulin [insulin level after eating]. In the regulation of lipid metabolism, berberine activity is better than metformin. By week 13, triglycerides and total cholesterol in the berberine group had decreased and were significantly lower than in the metformin group (P<0.05).”
Insulin resistance dropped by 45 percentThe second study in this same publication involved 48 adults already under treatment for type 2 diabetes with diet and one or more patent medications and/or insulin. Despite these various treatments, their type 2 diabetes was still poorly controlled. Diet and all medications had been the same in each individual for two months before berberine treatment was added, and remained unchanged for the three months of this second study.
After just 7 days, the added berberine (500 milligrams thrice daily) led to an average reduction in fasting blood sugar from 172 to 140 milligrams per deciliter, and average post-prandial blood sugar had declined from 266 to 210 milligrams per deciliter.
During the second week of added berberine, average fasting blood sugar dropped to 135 milligrams per deciliter, and postprandial glucose to 189 milligrams per deciliter. The researchers reported that these improvements were maintained for the rest of the three month study.
In addition, hemoglobin A1c decreased from 8.1 percent to 7.3 percent, fasting insulin decreased by 28 percent, insulin resistance was reduced by 45 percent, and total and low-density (LDL) cholesterol were both significantly reduced.
The researchers wrote that in their study of newly diagnosed diabetics who took berberine or placebo alone, “[n]one of the patients suffered from severe gastrointestinal adverse events when berberine was used alone.”
By contrast, the researchers wrote about the poorly controlled diabetics who added berberine to their on-going patent medication treatment: “Incidence of gastrointestinal adverse events was 34.5 percent during the 13 weeks of berberine…combination therapy.”
These adverse events included diarrhea in 10 percent, constipation in 7 percent, flatulence in 19 percent, and abdominal pain in 3.4 percent. The side effects were observed only in the first four weeks in most patients. In 24 percent, berberine dosage was decreased from 500 to 300 milligrams thrice daily because of gastrointestinal adverse events, and all of these side effects disappeared within one week.
The researchers concluded, “In summary, berberine is a potent oral hypoglycemic [blood sugar lowering] agent with modest effect on lipid metabolism. It is safe and the cost of treatment by berberine is very low.”
Better blood sugar control…and a few pounds shedIn a second publication, other researchers described results achieved by 116 individuals with type 2 diabetes and cholesterol and triglyceride abnormalities who participated in a randomized, double-blind trial that compared 500 milligrams of berberine taken twice daily with placebo, also taken twice daily.2 In the berberine group, average fasting blood sugar decreased from 126 to 101 milligrams/deciliter.
Two hours after a standardized glucose challenge, blood sugars decreased from an average 216 to an average 160 milligrams per deciliter. Average hemoglobin A1c decreased from 7.5 percent to 6.6 percent, average triglycerides decreased from 221 to 141 millgrams per deciliter, average total cholesterol decreased from 205 to 168 milligrams per deciliter, and average LDL-cholesterol (“bad” cholesterol) decreased from 125 to 97 milligrams per deciliter.
These researchers also reported “secondary outcomes.” Body weight decreased from an average 151 pounds to an average 146 pounds with berberine, a significantly greater fall (five pounds) than in the placebo group, who went from an average 158 pounds to an average 155 pounds, a loss of three pounds. A greater reduction of body mass index (BMI) was also found at three months in the berberine group than in the placebo group. Systolic blood pressure decreased from an average of 124 to 117 and diastolic blood pressure decreased from an average of 81 to 77 in those treated with berberine, exceeding the fall from 126 to 123 systolic and from 83 to 80 diastolic in those who took the placebo.
Side effects were few and mostly transient in the berberine group. Tests were done for kidney and liver function, as well as blood counts and electrolytes. Mild to moderate constipation occurred in five participants receiving berberine and one participant in the placebo group. Constipation “cleared up” in three of the five taking berberine and the one in the placebo group. The other two in the berberine group reduced their quantity of berberine by half to 250 milligrams twice daily, which relieved the constipation. Three measured liver enzymes (for the technically inclined AST, ALT, and GGT) all decreased to within the normal range.
How berberine does the jobSo how does berberine improve blood sugar control? Much of the answer involves the effect of berberine on insulin and insulin regulation. Some of the rest is explained by berberine’s indirect effect on blood sugar regulation through its effect on little-known (to non-researchers) gastro-intestinal hormones termed “incretins.”
Berberine improves the action of insulin by activating an enzyme (for the technically inclined, AMP-activated protein kinase, or AMPK) which helps regulate the cellular uptake of glucose, the oxidation (“burning”) of fatty acids and the synthesis of glucose transporter 4 (GLUT4), the insulin-regulated glucose carrier found in fat and skeletal and cardiac muscle that is responsible for moving glucose from the bloodstream into cells.3-6 GLUT 4 is found only in muscle and fat cells, the major tissues in the body that respond to insulin.
Berberine increases the “expression” (number and activity) of insulin receptors.7,8 The increase in number and activity of course enables the same amount of insulin to be more effective than before. Another way of describing this activity of berberine is “decreasing insulin resistance.” Other researchers have reported that berberine inhibits an enzyme (for the technically inclined, protein tyrosine phosphatase 1B, or PTP1B) which in turn inhibits the insulin receptor.9 When the insulin receptor isn’t inhibited as much, it can of course function better, and the net result is that insulin can “work” better.
“Incretins” are hormones secreted by our stomachs and intestines that simultaneously increase the amount of insulin and inhibit the amount of glucagon (a pancreatic hormone which “opposes” insulin) released from the pancreatic islet cells after eating, even before blood sugar levels rise. (It’s like an “anticipatory” action so more insulin—and less glucagon—will be immediately available when the glucose starts to rise in the blood.) Incretins also slow the rate of absorption of nutrients into the blood stream by slowing stomach emptying; this may indirectly reduce food intake.
Another way in which berberine regulates blood sugar is by increasing the secretion of one of the major incretins, glucagon-like peptide 1 (GLP-1).10
However, the actions of GLP-1 and other incretins to increase insulin release, lower glucagon release, and help regulate blood sugar are normally rapidly negated by another enzyme called DDP-4 (for the technically inclined, dipeptidyl peptidase 4). Yet another aspect of the blood sugar regulating action of berberine is its ability to inhibit DDP-4.11 When DDP-4 is inhibited, GLP-1 and other gut-secreted incretins aren’t broken down as rapidly, so they can continue to stimulate insulin and inhibit glucagon release significantly longer.
Are you a type 2 diabetic taking one of these medicines?The Lancet, considered to be one of the world’s “top” medical journals, published an editorial titled “Individualized incretin-based treatment for type 2 diabetes” in the August 7, 2010 edition. The author wrote, “All GLP-1 receptor agonists [molecules which stimulate the receptor for the incretin hormone GLP-1, which helps regulate blood sugar] that are “approved” [quotation marks added] or in development for the treatment of type 2 diabetes cause nausea, vomiting, and sometimes diarrhea in a substantial proportion of patients.”
He continued by observing that GLP-1 can help regulate blood sugar without these effects—which should be rather obvious because our own internally secreted GLP-1 doesn’t cause any of these problems! But rather than recommend that natural GLP-1—or berberine, which stimulates GLP-1—be used instead of “approved” or “under development” patent medicines, he instead suggests that researchers look into why the patent medications cause these problems, as this would “pave the way to an even more impressive exploitation of the incretin-based treatment strategy.”
Exploitation is exactly the correct word to describe this point of view, which ignores completely the much safer and considerably less expensive molecules found in our bodies and in Nature, and continues to pursue the development, sale, and use of prohibitively expensive patent medicine substitutes with much greater incidence of so-called “side” effects—which are actually part of the real effects of these never-before-found-on-planet-Earth (extraterrestrial, space alien) molecules.
But it’s your body and your health! If you have type 2 diabetes and are being “treated” with Januvia®, Victoza®, or Byetta®—which all affect the incretin-driven blood sugar regulatory system—consider switching to berberine at 500 milligrams three times daily. There’s ample scientific evidence to support such a change! Make sure to work with a physician skilled and knowledgeable in nutritional and natural medicine.
Thousands of years of use, and still largely ignoredBerberine is a major active component of the herb Coptis chinensis (Huang-lian), which—according to one research group—has been used in China to treat what is now identified as type 2 diabetes for literally thousands of years.
According to another research group, its blood sugar lowering effect was noticed when it was given to type 2 diabetic individuals to treat diarrhea. After the isolation of the berberine molecule itself, one of the first publications describing its use to lower blood sugar in type 2 diabetics was published in China in 1988.12 This and two subsequent research papers published in 200413 and 200514 found significant reductions in fasting and after-eating blood sugar control, and one also found significant reductions in cholesterol and triglycerides. Only one case of constipation (but no other adverse effects) was reported.
However, despite the safe and effective results reported, these studies suffered from the “defect” of not being placebo-controlled, and were (and are presently) only available in Chinese, so no one noticed them—with the possible exception of patent medicine companies working to make a patentable un-Natural molecule “analog” to berberine, and they won’t tell!
But the research studies you’ve already read about were “controlled,” and compared berberine directly with placebo or the number one established patent medication, metformin (Glucophage®, Glucophage XR®, Glumetza®, Fortamet®, Riomet®), or used berberine in addition to patent medication treatment—and all proved berberine to be clinically effective.
If you have type 2 diabetes and are using any patent medication, consider consulting a physician skilled and knowledgeable in natural and nutritional medicine and switching to berberine. Of course, there are many other natural techniques which can also be used to regulate and even normalize blood sugar in type 2 diabetes, including diet, exercise, vitamins, minerals, and other botanicals. It appears, however, that berberine can be a major tool, with fewer and less severe adverse effects than patent medications.
Tahoma Clinic physicians presently recommend Berberine Advantage (Tahoma Clinic Dispensary) or Berberine Plus™ (True Botanica™), 500 milligram capsules, each of which contain 485 milligrams of berberine itself. They are available at natural food stores, compounding pharmacies, and the Tahoma Clinic Dispensary (see “Resources,” page
. Although I work with Tahoma Clinic Dispensary, I am not affiliated with True Botanica™. JVW
Thank you to Ronald Steriti, N.D., who researched and organized the material used in this article!
Peppermint oil helps relieve irritable bowelMost of us have experienced the typical symptoms of irritable bowel syndrome at one time or another. It is characterized by abdominal pain or discomfort with bloating, gas, diarrhea, or constipation (or even diarrhea and constipation alternating with each other over time). But this most common digestive problem doesn’t even have a proper diagnosis. Irritable bowel syndrome (IBS) is only diagnosed after all medical tests for digestive diseases come back negative.
What causes IBS is not fully understood. Stress certainly plays a key role, as does spasm in the gut and changes in gut motility (how fast food moves through the digestive process). Conventional drugs generally offer only mild relief, sometimes at the cost of significant side effects. Amazingly there is now convincing scientific evidence that the best available relief for IBS symptoms comes in a natural form: the oil distilled from peppermint leaf.
Ancient wonder meets modern scienceOur relationship with peppermint certainly has a long history. The mints, including peppermint, are among the oldest European herbs used for both cooking and medicine. The Greeks and Romans crowned themselves with peppermint at their feasts and adorned their tables with it. Their cooks flavored both their sauces and their wines with its essence. Peppermint was cultivated by the Egyptians, but only came into general use in Western Europe in the 18th century where it was used in home remedies to relieve the stomach and intestines of gas associated with the consumption of certain foods.
The essential or volatile oil of peppermint is distilled from the fresh leaf by driving steam through it. (Here the word “essential” derives from essence, as in perfumery.) Both the oil vapor and the steam condense in the collection tank. Since they don’t mix, the oil is readily separated. It is rich in menthol, which gives a fresh cooling sensation when inhaled or put on the skin.
Human studies have found that peppermint oil is a powerful relaxant of gut muscle. This has been shown very clearly in some colonoscopy experiments. When peppermint oil was injected along the biopsy channel of the colonoscope in 20 patients, it relieved colon spasm within 30 seconds, allowing easier passage of the tube.
Due to the potential irritant effect of neat (undiluted) peppermint oil, a diluted suspension was used with equally good effects.1 The direct administration of 15 drops of peppermint oil in 30 mL of water into the stomachs of 27 volunteers caused relaxation of the lower esophageal sphincter. But gastroesophageal reflux occurred in 25 out of these 27 people within one to seven minutes of peppermint administration.2 (There go the after dinner mints!)
This relaxing of the esophageal sphincter is a well-known property of peppermint. Herbs that relax sphincters and thereby allow the passage of gas are known as carminatives. Several other clinical trials have shown that direct administration of peppermint oil reduces gastric and colonic spasm and is safe and useful for upper gastrointestinal endoscopy, colonoscopy, and double contrast barium enema examination (DCBE).
Relief for almost 90 percent of patientsOne study looked at the efficacy of peppermint oil (10 mL of a 1.6 percent emulsified solution) as an antispasmodic for DCBE. Oral doses of this peppermint oil emulsification reduced spasm of the esophagus, lower stomach, and duodenum and improved the diagnostic quality of the procedure without requiring the injection of an antispasmodic drug.3
These effects were confirmed in a large study where 409 patients received about 200 mL of an oil-in-water emulsion containing 1.6 mL of peppermint oil. This was given via a colonoscope using a hand pump.4 An antispasmodic effect was seen in 88.5 percent of treated patients versus 33.3 percent of 36 controls. Onset was in seconds and the activity lasted for at least 20 minutes. Results from a randomized, double blind, controlled trial in 100 patients found that direct administration of a peppermint oil solution had superior efficacy and fewer side effects than injection of the antispasmodic drug hyoscine-N-butylbromide during upper endoscopy.5
These spasm-relieving effects of peppermint oil are probably the main reason why it is so clinically effective in IBS. As already mentioned, there is a high level of scientific evidence that it works well. All these studies used an enteric-coated capsule. This means that the capsule will not dissolve in the stomach and so the carminative effect of the oil that can lead to reflux is avoided.
IBS pain—relieved without drugsA review published in 2005 found 16 clinical trials of peppermint oil in IBS dating from 1979 to 1997.6 These trials all showed that peppermint oil was able to reduce most IBS symptoms, but especially pain, and worked as well as conventional antispasmodic drugs. The dose was 1 to 2 capsules three times a day with each capsule containing between 180 and 200 mg of peppermint oil.
The trials published since 1997 add further weight to the positive findings of this 2005 review. For example, an Italian study assessed the impact of enteric-coated peppermint oil or placebo for three months in 178 patients with IBS.7 Using a double blind, placebo-controlled design there was a significant advantage observed for peppermint oil over placebo in terms of overall symptoms, with 80 percent improved versus 36 percent for placebo.
Another Italian study over four weeks used a similar design in a trial involving 57 patients with IBS.8 Symptoms evaluated included abdominal bloating, abdominal pain, diarrhea, constipation and passage of gas or mucus. By the end of the trial 75 percent of patients taking peppermint oil achieved a greater than 50 percent reduction in symptom score, compared to 39 percent in the placebo group.
The most powerful evidence for any medical treatment comes from a process known as meta-analysis. This is where the results of several clinical trials are pooled together using statistics to create one big trial. Recently this was done for trials of peppermint oil, fiber, and antispasmodic drugs in relieving IBS (a separate analysis for each treatment).9 The analysis found that the least clinical benefit came from fiber, although it was still better than placebo. The next best treatment was the drugs, but best of all was peppermint oil. KB
A convenient oversight from Consumer Reports®In last April’s issue of Nutrition & Healing, I started the article “The amazing supplement news you won’t hear anywhere else” this way: “Bad news about dietary supplements—most frequently flawed studies or other bad science intended to ‘debunk’ or scare you about them—is often found on the front pages of daily newspapers…” In August, the media were doing it again: TV, radio, internet, local newspapers were all trumpeting the attack article in the September 2010 issue of Consumer Reports®, the otherwise well-balanced but uninformed-about-supplements publication of the Consumers Union.
Specifically, in one article, after discussing the bad effects of a single mislabeled supplement out of 54,000 sold (their reported number), Consumer Reports went on to list its self-named “dirty dozen” supplements: aconite, bitter orange, chaparral, colloidal silver, coltsfoot, comfrey, country mallow, germanium, greater celandine, kava, lobelia, and yohimbine.
But nowhere in the entire article did they note the report about total deaths from dietary supplements in 2008, compiled by the American Association of Poison Control Centers’ National Poison Data System.1 Their 174-page publication in the medical journal Clinical Toxicology reports that there was not even one death caused by a dietary supplement in 2008!
Although it is certainly possible for any manufacturer of supplements to make a labeling error, and it’s also possible for an individual to have an adverse reaction to nearly anything, it’s also entirely true that there was not one death in all of 2008 from aconite, bitter orange, chaparral, colloidal silver, coltsfoot, comfrey, country mallow, germanium, greater celandine, kava, lobelia, or yohimbine. Somehow, Consumer Reports overlooked this important data from a very reliable source.
Your most pressing health questions…answered!Department of “Duh”
Surprise! Space alien molecules are bad for youSummer 2010 was “silly season” for “mainstream” medical researchers reporting adverse effects or very little effect of nutrient supplementation. Perhaps they should consult one of the relatively few MD- or DO-physicians skilled and knowledgeable in nutritional or natural therapies, or (heaven forbid!) any ND-physician, a compounding pharmacist, a non-ADA dietician/nutritionist, or even an experienced worker in a natural food store before spending what is likely to be hundreds of thousands or even millions of dollars on useless research.
In July, the British Medical Journal reported a review (“meta-analysis”) of 15 research studies, in each of which 100 or more individuals took calcium supplements of 500 milligrams or more daily. Their conclusion? “Calcium supplements (without co-administered vitamin D) are associated with an increased risk of myocardial infarction.”1
I’ve a question for these researchers: Would you like a side order of chalk? I mean, that’s what we’re talking with pure calcium carbonate. Who in their right mind would eat anything containing just calcium (with carbonate), anyway? Even allopathic (MD) medical students are taught that calcium often “opposes” magnesium in muscle function: Calcium aids muscle contraction (think blood vessel spasm, less blood flow, and possible “heart attack”), and magnesium aids muscle relaxation (think blood vessel dilation, more blood flow, less chance of heart attack). Calcium is found with magnesium—and zinc and copper and manganese and molybdenum and boron and selenium—in bone. No one eats chalk!
No DO- or MD-physician skilled and knowledgeable in nutritional or natural therapies, no ND-physician, no compounding pharmacist, no non-ADA dietician/nutritionist, no experienced worker in a natural food store, and no one taking care of his or her own health would think of taking any significant quantity of calcium without magnesium.
So who would make this mistake? Apparently these “mainstream” medical researchers, the “mainstream” researchers who conducted the 15 research studies they reviewed, and the research volunteers who trusted these “mainstream” researchers to know what they were doing. And the result? Let’s re-state the conclusion of this review to reflect “all the facts, ma’am!”: “Calcium supplements [given alone, without magnesium, vitamin D, or any other minerals, at all] are associated with an increased risk of myocardial infarction.” Duh!
A daily dose of margarine?Then in August came an equally lame research report. The opening lines of the Associated Press article describing this research (done with over 4,837 adults ages 60–80 who’d suffered heart attack in the prior ten years) nearly “say it all” about the level of nutritional expertise represented by these researchers: “Eating more heart-healthy omega-3 fats provided no additional benefit in a study of heart attack survivors who were already getting good care, Dutch researchers report. After nearly 31/2 years, there was no difference in deaths, heart attacks and other heart problems between those who ate margarine with added omega-3 fatty acids and those who didn’t, the study found.”2
Double duh! Even New York City bureaucrats and politicians who banned trans-fats know that margarine containing trans-fatty acid is bad for the heart! How can any 21st century research scientist seriously write “already getting good care” and “ate margarine” in the same paragraph? And not just a little margarine, either. The researchers prescribed 4 teaspoonsful (18 grams, or almost 2/3 of an ounce) a day for those 31/2 years! Do you know anyone who eats almost 2/3 of an ounce of trans-fatty acid containing margarine a day, every day?
And how much fish oil did the researchers prescribe? A “grand” combined total of 400 milligrams EPA and DHA—smaller than the amount found in the average single fish oil capsule! 400 milligrams of EPA and DHA versus 18,000 milligrams of margarine! And even though the researchers also prescribed 2,000 milligrams of ALA—which has a beneficial effect against cardiovascular disease, but considerably less than EPA and DHA—all that margarine overcame any potentially beneficial effects of the small amounts of EPA, DHA, and the “weaker” ALA.
Were research subjects put in harm’s way?There may also be a bit of an ethical question about this research. These 4,837 older individuals had already had one heart attack, and the researchers recruited them between 2002 and 2006, when they surely must have known the extra risk involved in eating margarine every day, especially that much. Unfortunately this possible ethical lapse wasn’t addressed in either the research paper or the newspaper report.
To make matters worse, this failed-before-it-began study was partially funded by you and me—taxpayers—via the National Institutes of Health, whose funding officials should know the health dangers of trans-fatty acid containing margarine!
If these researchers had really wanted to investigate the effects of omega-3 fatty acids against cardiovascular disease, they could have omitted the margarine and recommended an adequate quantity of omega-3 fatty acids to these trusting older people.
So much for “mainstream” research concerning nutrients. Remember the fuss a few years ago about vitamin E causing heart attacks? Those researchers used only a vitamin E fraction, alpha-tocopherol, leaving out the gamma, beta, and delta tocopherols which are part of the over-all vitamin E complex found in Nature. And gamma tocopherol is most important to the heart.
It’s becoming more and more obvious that research into nutrients should be left to real experts in the field. The medical “mainstream” might best stick to researching patent medications.
Natural Response
Get the most out of BHRTDear Dr. X,
We have two questions regarding hormones:If estradiol (E2) is the most abundant in women and estriol (E3) is associated mostly with pregnancy, why then do we give “Bi-est” (an 80/20 or 70/30 combination of E3 and E2)? How are we copying Nature if we do that?
If the body normally makes 0.5 milligrams of estrogen a day why do we go as high as 2.5 or even 5 milligrams daily when we replace? We are aiming to copy nature—so why is this correct?
—A.S., RPA-C
Dr. x: Thank you for asking! Estradiol (E2) is the most potent female hormone, not the most abundant. As shown by literally tens of thousands of 24-hour urine analyses, estriol (E3) is usually (but not always) produced by women’s bodies in greater quantities than the sum of estradiol and estrone [E1].
Another part of the answer involves safety when prescribing BHRT. Although in most women, E2 (a pro-carcinogen) “metabolizes through” to a greater quantity of E3 (an anti-carcinogen), thus maintaining an anti-carcinogenic balance, in a significant minority of women this transformation doesn’t happen adequately, leaving them with a pro-carcinogenic balance. For this reason, I decided in the 1980s that it was safest to insure an anti-carcinogenic E3/E2 balance for 100 percent of all menopausal and post-menopausal women using BHRT by prescribing Bi-Est (80 percent E3/20 percent E2). This actually does copy Nature’s normal healthy metabolic function while avoiding one of Nature’s un-healthy metabolic functions. There’s no point in potentially copying a metabolic error for some women, is there?
We use quantities of Bi-Est as high as needed to achieve normal physiologic levels—as actually measured in blood and urine—of estrogens as well as all of the other hormones used in BHRT. We are copying Nature by achieving physiologic levels, whatever the quantity needed to achieve them.
Both your questions help illustrate why follow-up tests to monitor results are just as important as the clinical evaluation for maximal safety and efficacy of BHRT. Thank you!
References
Department of “Duh” Summer of mainstream mistakes1 Bolland MJ, Avenell A, Baron JA, Grey A, Maclennan GS, Gamble GD, Reid IR. Effect of calcium
supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. BMJ. 2010 Jul 29;341
2 Nano S. Study: More omega-3 fats didn’t aid heart patients. Associated Press. 2010 Aug 29.
A convenient oversight from Consumer Reports®1 Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Giffin SL. 2008 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 26th Annual Report. Clinical Toxicology (2009). 47, 911-1084. The full text article is available for free download at
http://www.aapcc.org/dnn/Portals/0/2008annualreport.pdf . Vitamins statistics are found in Table 22B, journal pages 1052-3. Minerals, herbs, amino acids and other supplements are in the same table, pages 1047-8.
Get your type 2 diabetes under control…without a single drug!1Yin, J., H. Xing, et al. (2008). Efficacy of berberine in patients with type 2 diabetes mellitus Metabolism 57(5): 712-7.
2 Zhang, Y., X. Li, et al. (2008). Treatment of type 2 diabetes and dyslipidemia with the natural plant alkaloid berberine. J Clin Endocrinol Metab 93(7): 2559-65.
3 Turner, N., J. Y. Li, et al. (2008). Berberine and its more biologically available derivative, dihydroberberine, inhibit mitochondrial respiratory complex I: a mechanism for the action of berberine to activate AMP-activated protein kinase and improve insulin action. Diabetes 57(5): 1414-8.
4 Lee, Y. S., W. S. Kim, et al. (2006). Berberine, a natural plant product, activates AMP-activated protein kinase with beneficial metabolic effects in diabetic and insulin-resistant states. Diabetes 55(
: 2256-64.
5 Ma, X., T. Egawa, et al. (2010). Berberine-induced activation of 5′-adenosine monophosphate-activated protein kinase and glucose transport in rat skeletal muscles. Metabolism.
6 Hwang, J. T., D. Y. Kwon, et al. (2009). AMP-activated protein kinase: a potential target for the diseases prevention by natural occurring polyphenols. N Biotechnol 26(1-2): 17-22.
7 Zhang, H., J. Wei, et al. (2009). Berberine lowers blood glucose in type 2 diabetes mellitus patients through increasing insulin receptor expression. Metabolism 59(2): 285-92
8 Kong, W. J., H. Zhang, et al. (2009). Berberine reduces insulin resistance through protein kinase C-dependent up-regulation of insulin receptor expression. Metabolism 58(1): 109-19.
9 Chen, C., Y. Zhang, et al. (2010). Berberine inhibits PTP1B activity and mimics insulin action. Biochem Biophys Res Commun 397(3): 543-7.
10 Yu, Y., L. Liu, et al. (2009). Modulation of glucagon-like peptide-1 release by berberine: in vivo and in vitro studies. Biochem Pharmacol 79(7): 1000-6.
11 Al-masri, I. M., M. K. Mohammad, et al. (2009). Inhibition of dipeptidyl peptidase IV (DPP IV) is one of the mechanisms explaining the hypoglycemic effect of berberine. J Enzyme Inhib Med Chem 24(5): 1061-6.
12 Ni YX (1988) Therapeutic effect of berberine on 60 patients with type II diabetes mellitus and experimental research [article in Chinese]. Zhong Xi Yi Jie He Za Zhi 8:711–713
13 Wei J, Wu J, Jiang J, Wang S, Wang Z (2004). Clinical study on improvement of type 2 diabetes mellitus complicated with fatty liver treatment by berberine [article in Chinese]. Zhong Xi Yi Jie He Ganbing Za Zhi 14:334–336
14 Xie P, Zhou H, Gao Y 2005 The clinical efficacy of berberine in treatment of type 2 diabetes mellitus [article in Chinese]. Chin J Clin Healthcare 8:402–403
Peppermint Oil Helps Relieve Irritable Bowel1Leicester RJ, Hunt RH. Lancet 1982; 2(8305): 989.
2 Sigmund CJ, McNally EF. Gastroenterology 1969; 56(1): 13-18.
3 Mizuno S, Kato K, Ono Y et al. J Gastroenterol Hepatol 2006; 21(
: 1297-1301.
4 Asao T, Mochiki E, Suzuki H et al. Gastrointest Endosc 2001; 53(2): 172-177.
5 Hiki N, Kurosaka H, Tatsutomi Y et al. Gastrointest Endosc 2003; 57(4): 475-482.
6 Grigoleit HG, Grigoleit P. Phytomed 2005; 12(
: 601-606.
7 Capanni M, Surrenti E, Biagini MR et al. Gazz Med Ital-Arch Sci Med 200; 164: 119-126.
8 Cappello G, Spezzaferro M, Grossi L et al. Dig Liver Dis 2007; 39(6): 530-536.
9 Ford AC, Talley NJ, Spiegel BMR et al. BMJ 2008; 337; a2313.
10 Leicester RJ, Hunt RH. Lancet 1982; 2(8305): 989.
11 Sigmund CJ, McNally EF. Gastroenterology 1969; 56(1): 13-18.
12 Mizuno S, Kato K, Ono Y et al. J Gastroenterol Hepatol 2006; 21(
: 1297-1301.
13 Asao T, Mochiki E, Suzuki H et al. Gastrointest Endosc 2001; 53(2): 172-177.
4 Hiki N, Kurosaka H, Tatsutomi Y et al. Gastrointest Endosc 2003; 57(4): 475-482.
5 Grigoleit HG, Grigoleit P. Phytomed 2005; 12(
: 601-606.
6 Capanni M, Surrenti E, Biagini MR et al. Gazz Med Ital-Arch Sci Med 200; 164: 119-126.
7 Cappello G, Spezzaferro M, Grossi L et al. Dig Liver Dis 2007; 39(6): 530-536.
8 Ford AC, Talley NJ, Spiegel BMR et al. BMJ 2008; 337; a2313.
