Archive for Soy isoflavones
Importance of Equol—A Clue to Effectiveness of Soy Isoflavones
We see a familiar concept here. Soy isolflavones need to be acted on by beneficial bacteria in the gut to produce equol–a nonsteroidal estrogen-like compound that is believed to be one of the most potent antioxidants in this class. This may explain some of the discrepancies in soy benefit studies and is further proof for a holistic approach to health that would include lifestyle changes to support healthy bacterial flora. We see this same concept with soluble fiber and colon cancer–the fiber needs to be acted on by beneficial bacteria to produce butyrate to protect the colonocytes.
Nutrition.org — Abstracts: Setchell et al. 132 (12): 3577
Adrenocortical Effects of Oral Estrogens and Soy Isoflavones
Just in case this email gets to an ob/gyn and they think I don’t know what I’m talking about… This article (which is a monkey study) finds that both oral contraceptive and conjugated equine estrogens (i.e. Premarin) mess with the adrenal glands in a negative way, producing too much cortisol and not enough DHEA. And, since this imbalance is well known to contribute to insulin resistance, do I need say any more?
JCEM — Abstracts: Wood et al. 89 (5): 2319 -
Soy isoflavones improve lipids in normal & mildly hypercholesterolemia
Soy is believed to act through several mechanisms (most centered on the liver) to lower cholesterol levels. The effect in this study was mild, but, as with any functional approach, with added exercise, lowering of refined carbs (high insulin will stimulate HMG-CoA reductase..the enzyme that makes cholesterol), nutrients designed to stimulate healthy liver and gall bladder function (to aid in the elimination of cholesterol through the feces) and avoidance of saturated fat and I’m the effect is no longer mild.
AJCN — Abstracts: Wangen et al. 73 (2): 225 http://www.ajcn.org/cgi/content/abstract/73/2/225
The Effect of Soy Consumption on 2:16-Hydroxyestrone Ratio in Postmenopausal Women Depends on Equol Production Status but is not influenced by Probiotic Consumption
Here’s some background…the body metabolizes estrogens down several pathways. The “2″ pathway is considered protective for certain types of cancer while the “16″ pathway is damaging. It is known that equols, compounds produced by bacterial conversion of soy isoflavones in the gut, shift the metabolization of estrogen to the 2 pathway (so does indole-3-carbonol from cruciferous veggies).
So, the idea in this study was to give probiotics with soy to see how much of an effect on equol levels was seen. There seems to be a subset of women that respond positively to this approach, but the researchers were not able to identify specifics. I do have a question for the more research-minded readers out there…
This study used a 2 week washout period. How can you get a washout period using probiotics? All things being healthy–the probiotics should maintain in the GI tract. I wonder how much this influenced the results?
Dietary Fiber and C-Reactive Protein.
I’ve said it before…why all the ruckus trying to find a drug that will lower CRP levels? We already have many natural approaches that will lower CRP levels–exericse, avoiding refined carbs, fish oils… Many clinicians are still not ordering CRP levels for their patients at high risk of heart disease. As far as I’m concerned, the evidence is very strong that CRP is a risk factor for many chronic diseases. I always run CRP levels in my office anytime I requiest bloodwork. nutrition.org — Abstracts: Ajani et al. 134 (5): 1181 - Click here for more information.
Hypovitaminosis D associated with insulin resistance and beta cell dysfunction.
The authors state that the relationship between Vit D and diabetes is well recognized, but this is the first I’ve heard of this relationship. Vit D (in it’s active form 25-hydroxyvitamin D) has been all over the medical literature in the past few months. What I do know, is that sunlight exposure has gotten such a bad rap in the past few years because of the increase in skin cancer. So people are staying out of the sun and wearing sunblock. I’m not saying to go bake for 3 hours in the AZ sun with baby oil on, but 10-15 minutes a day of good strong sunshine is part of a healthy lifestyle. AJCN — Abstracts: Chiu et al. 79 (5): 820 - Click here for more information.
Sarcopenia and increased adipose tissue infiltration of muscle in elderly.
The inflitration of fat into skeletal muscle is one of those subtle changes that occurs over time that can have a dramatic effect on long term health. Try this scenario–a young woman skips breakfast in an attempt to cut calories and lose weight. And she is successful. However, some of the weight lost has been replacement of lean muscle mass with intramuscular fat. She even looks like she lost weight. But she has made a devastating change to her biochemical makeup. The weight will come back on–with less lean muscle mass it is inevitable–and each cycle it gets harder and harder to lose the weight. AJCN — Abstracts: Song et al. 79 (5): 874 - Click here for more information.
Selective serotonin reuptake inhibitors in childhood depression: systematic review of published versus unpublished data.
This issue has really blown up lately. With the increasing use of psychoactive medications to our children (which I think is absolutely unacceptable except in the most severe cases) the safety of this class of medications is not known. It turns out that many of these drugs had studies done that showed a negative risk-benefit ratio with some studies showing an increase in suicide rates in medicated kids. But these studies were conveniently never published which led to a favorable outcome when one looked ONLY at the published studies. While this type of shenanigans is fine for GM or Honeywell or some other big company, this is our future we are messing with. For those of you reading this with small children at home–could you possibly imagine giving your child a powerful drug that affects the mind when we do not know what the long term damage may be? Or worse yet, the damage is known but hidden? Where is this glorius FDA that we want to put in charge of our vitamins? (editorial on this topic The Journal : Back Issues Back Issues).
US junior doctors found to be ignorant of drug companies’ tactics.
Okay. Most educated people on the street know or have some idea that the pharmaceutical companies use money and gifts to influence the prescribing behavior of doctors, and that these methods are very effective. However, residents were unaware of this behavior? Huh? No wonder it’s effective. bmj.com Spurgeon 328 (7447): 1032 - Click here for more information.
The Temporal Relationship Between the Onset of Type 1 Diabetes and Celiac Disease: A Study Based on Immunoglobulin A Antitransglutaminase Screening.
This is an interesting study. Here’s how it works. We have blood tests that help determine whether a patient has an allergy to gluten containing grains (celiac disease). Children with Type I diabetes have a strong association with celiac disease. This study finds that the celiac disease can be identified before the onset of Type I diabetes. This is significant because there are interventions that can be effective at slowing or stopping the beta cell destruction in the pancreas such as niacinamide. So, if we have an easy blood test we may be able to intervene and stop the progression to diabetes. Pediatrics — Abstracts: Peretti et al. 113 (5): e418 - Click here for more information.
Adverse Effects of Modest Sleep Restriction on Sleepiness, Performance, and Inflammatory Cytokines.
I know I’m guilty here. We all know that sleep is very important and is a stress on the body, but to increase inflammation is definately news to me. And considering that inflammation plays a role in just about every chronic disease we know of, getting a good night’s sleep becomes even more important. I would like to see if the use of drugs for sleep, such as Ambien, would avoid the increase in inflammatory markers since is does interfere with the deepest levels of sleep. JCEM — Abstracts: Vgontzas et al. 89 (5): 2119 - Click here for more information.
Increased CRP in Polycystic Ovarys: Marker of Cardiovascular Disease.
This is another good example of the intricate web that is physiology. While change is occurring but slow, many ob/gyns will treat PCOS with the birth control pill, which will worsening insulin sensitivity. If treated this way, the physician is missing the boat entirely, and will leave the physiological imbalance we know as Syndrome X to run rampant and destroy the patient’s health. JCEM — Abstracts: Boulman et al. 89 (5): 2160 - Click here for more information.
Adrenocortical Effects of Oral Estrogens and Soy Isoflavones.
Just in case this email gets to an ob/gyn and they think I don’t know what I’m talking about… This article (which is a monkey study) finds that both oral contraceptive and conjugated equine estrogens (i.e. Premarin) mess with the adrenal glands in a negative way, producing too much cortisol and not enough DHEA. And, since this imbalance is well known to contribute to insulin resistance, do I need say any more? JCEM — Abstracts: Wood et al. 89 (5): 2319 - Click here for more information.
The “fiction” of primary prevention: Role of IVUS in identifying early atherosclerosis.
This is a review of the presentation of Dr. Stephen Nissen at the European Atherosclerosis Society 2004 meeting. And, while it is really no surprise to anyone who cracks a medical journal at least semi-annually, he shocked attendees by stating that 75% of attendees most likely has coronary artery disease that can be identified by intravascular ultrasound and that by the time we identify the problem, it has been ongoing for decades already. However, he addresses “primary prevention” as what cardiologist are doing–to me this is nowhere near “primary.” Addressing lifestyle factors that contribute to inflammation and promoting diets low in refined carbs and trans fats but high in whole grains and fruits and veggies can have a huge impact long before any symptoms might have appeared. This is true primary prevention. Click here for more information.
This review is from Heartwire at theheart.org: If a picture is worth a thousand words, then intravascular ultrasound (IVUS) speaks volumes for physicians looking to identify early plaque development in atherosclerosis. Some patients, through the eyes of the ultrasound, are revealed to be in the early stages of atherosclerosis, with fatty plaques lining arteries once thought to be healthy, says one imaging expert.
In fact, according to Dr Steven Nissen (Cleveland Clinic, OH), primary prevention no longer exists. “In many patients, we know that by the time we recognize the disease, it has moved through the entire arterial tree,” he said.It’s more than luminal narrowingNissen recently discussed IVUS and the key lessons learned from the imaging modality at the European Atherosclerosis Society 2004 meeting.Mechanical ultrasound of the vascular lumina involves the insertion of a rotating catheter, capable of 1800 rpm, or 30 times per second, explained Nissen. The catheter sends and receives ultrasound at 30 to 40 MHz to produce full-motion images of the artery in real time, allowing clinicians to see images of the artery at a full 30 frames per second.
“What is attractive about this technique, compared with carotid intima-media thickness, is that we see the whole 360° circumference of the artery,” said Nissen. “By moving the catheter longitudinally, we get to see slice-by-slice, in tomographic fashion, the entire atherosclerotic burden in the vessel.”During his session, Nissen said the ability of IVUS to detect atherosclerotic plaque within the luminal wall separates IVUS from conventional imaging techniques such as angiography. As much as 99% of all atherosclerotic plaque is extraluminal, growing in an outward fashion and, as a result, does not narrow the artery, he said.”The disease that we’re interested in is not observed in the vessel lumen, but rather it’s observed in the vessel wall,” said Nissen. “The issue here is that it is the behavior of the plaque in the vessel wall that determines the natural history and pathophysiology of the disease.”
Contrasting a supposedly healthy artery as viewed by angiography with the IVUS image that showed extensive plaques, Nissen told the European audience that atherosclerosis starts very early, most likely in the late teenage years and early twenties.”By the time we start to treat the patient the disease is everywhere. There is no such thing as primary prevention. It is pure fiction. It is always secondary prevention we’re talking about,” said Nissen. He added that at least 75% of his assembled audience likely has extensive coronary atherosclerosis, much to their chagrin. “It’s not a fun thought, but it’s really true,” he said.Dr Emilio Ros (Lipid Hospital Clinic, Barcelona, Spain), one of the meeting cochairs, agreed that IVUS shows some pretty “amazing” images but said the deposition of cholesterol into the arterial wall may be only controlled, rather than completely avoided.
“From the moment we’re born and start drinking breast milk, our arteries are beginning to line with plaques,” Ros told heartwire. “It’s what happens. We have an innate tendency to deposit cholesterol in our arteries. We don’t want to see enormous atherosclerosis in 40-year-old patients, but through lifestyle, we hope to delay this tendency to build up plaque.”
Ros said IVUS provides better visualization of disease, allowing physicians to aggressively target high-risk patients earlier, but such treatment comes with a cost. “This could be a very, very expensive opportunity,” he said. “IVUS is probably the best tool that we have today to assess risk,” Dr Michel Romanens (Rodiag Diagnostic Centers, Belchenstrasse, Switzerland) told heartwire. Speaking on the topic of risk prediction, Romanens said the most interesting marker that emerges from IVUS is the total plaque volume. Unfortunately, clinicians are still unable to identify the components of the plaque with IVUS, he said.”What Steve Nissen adds to the community of risk prediction is that he probably has the best tool, but it’s an invasive tool, and we can’t go putting catheters in everybody,” added Romanens. If I had a hammer. . . During his presentation, Nissen lamented the misguided direction of interventional cardiologists, quoting Mark Twain, who once remarked, “To a man with a hammer, everything looks like a nail.” With 99% of disease hidden from angiographic view, treating a narrowed artery with a stent fails to address the extensive underlying atheroma burden, he said. For this reason, many epidemiologic studies have failed to demonstrate any morbidity and mortality benefit with coronary stents.”Stenting doesn’t treat the disease in its entirety but rather treats about 1% of the disease,” said Nissen. “”You can’t treat the 1% of the plaque you see and expect to affect the other 99% you don’t. That’s the problem with this approach.”He added that when the disease first shows up as a luminal irregularity on the angiogram, as much as 80% of the coronary arterial tree is already atherosclerotic. Interestingly, Nissen also presented a sequence of IVUS images capturing plaque rupture. The series showed atheroma breaking from the arterial wall, emptying into the lumen, where it moved downstream.ApoA-1 Milano and REVERSALNissen noted that recent studies have changed his opinion about how to best treat atherosclerosis. Once believed to be a chronic, indolent progression of atheroma within the arteries, emerging research as shown the disease to be more dynamic than realized.
One pilot study, in which Nissen was lead investigator, tested recombinant apolipoprotein (Apo) A-1 Milano, an HDL mimetic, and found that weekly infusions of the agent over five weeks produced significant regression of coronary atherosclerosis in ACS patients. The REVERSAL study, again in which Nissen was lead author, showed that intensive lipid-lowering treatment with atorvastatin (Lipitor®, Pfizer) 80 mg daily halted the progression of atherosclerosis, whereas a moderate lipid-lowering regimen was associated with continued atherosclerosis progression. Both studies were previously reported by heartwire.”This gives me great hope for the future of antiatherosclerotic therapies because I believe that this disease is far more dynamic than we ever realized,” said Nissen. “We can regress the disease if we combine LDL-lowering therapies, HDL-raising therapies, and therapies that target inflammation. We’re going to start seeing a major regression of this disease.”Next up is an 1100-patient IVUS study investigating whether torcetrapib, a cholesteryl ester transfer protein inhibitor (CETP) that raises HDL cholesterol, can cause atherosclerotic disease regression. Enrollment is now completed and results are expected in two years, Nissen said.
The Relative Safety of Ephedra Compared with Other Herbal Products.
Alright, while I rarely recommend ephedra containing products in my office, I need to speak up on this issue. First of all, ephedra products are greatly overused and the potential for abuse is high. But, in all, there have been maybe 20 deaths associated with ephedra over its recorded history. Not to minimize 20 deaths, but Tylenol kills that many in a month, let alone over it’s recorded history and yet no one is screaming for Tylenol to be pulled from the shelves. Make no mistake–the attack on ephreda is only the beginning of a slippery slope to make supplements prescription items to be prescribe only by doctors who have little or no training in these products.
Annals of Internal Medicine: Abstract – Click here for more information.
NSAIDs as a Trigger of Clinical Heart Failure.
NSAIDs double the risk of heart failure in patients with a history of heart problems. Considering their widespread use, the number of patients affected by this association is probably close to staggering. All by themselves, NSAIDs are believed to cause some 16-19,000 deaths per year via GI bleeding (kind of beats 20 over a lifetime, huh?).
Click here for more information.
Plasma oxidized LDL: a predictor for acute myocardial infarction?
Remember that LDL cholesterol itself does not do damage to the body until it gets damaged itself through oxidation (sometimes termed oxysterols). Here we see the development of yet another tool to assess heart disease risk. Keep in mind that, even with high cholesterol, high intakes of antioxidants can serve to protect the LDL particle from being damaged.
Synergy Abstract – Click here for more information.
Amino Acids Strongly Enhances Insulin Secretion in Type 2 DM.
In patients with diabetes, the pancreas begin to putter out and ultimately produces less and less insulin (as opposed to syndrome X, where hyperinsulinemia is the damaging force). Many diabetic drugs are designed to force the pancreas to produce more insulin. Here we see that certain amino acids can have the same effects, thus giving dietary recommendations a strong therapeutic potential for treatment of diabetes. What is interesting is that the insulin response was strongest in a specific amino acid preparation along with a carbohydrate meal. This also puts a wrench in the works for those that say high protein diets work by lowering the body’s response to insulin.
Dia Care — Abstracts: van Loon et al. 26 (3): 625 – Click here for more information.
Blood Lead, BP, and Hypertension.
Heavy metals are widely overlooked by mainstream medicine despite heavy research into their affects on human health. Here we see links with hypertension. Of additional note on BP is cadmium (found mainly in cigarette smoke) which damages the kidneys and can lead to hypertension.
JAMA — Abstracts: Nash et al. 289 (12): 1523 – Click here for more information.
Magnesium, phospholipid and energy metabolism between migraine syndromes.
I found it very interesting when one of my patients with seizures consulted an ER doctor friend of hers about her seizures. He basically informed her that she needed to be on antiseizure medication (with a standing order for bloodwork to check liver enzymes every two weeks…) and nothing else had any effect. Apparently he hasn’t cracked a medical journal in several years, and sadly, when doctors display their ignorance on subjects they are not educated in it confuses patients and can compromise their adherence to recommendations. In this article we see that magnesium has an effect on hyperexitability of the cortex. This article relates these findings to the aura of a migraine, which is essentially seizure activity.
Synergy Abstract – Click here for more information.
Lack of significant genotoxicity of purified soy isoflavones (genistein, daidzein, and glycitein) in 20 patients with prostate cancer.
This article is interesting given the fact that men with history of prostate cancer and women with history of breast cancer are told to avoid soy products. However, the evidence seems to support the fact that soy compounds are not only non-harmful, but possibly show a benefit.
AJCN — Abstracts: Miltyk et al. 77 (4): 875 – Click here for more information.
Saw Palmetto for Prostate Disorders.
American Family Physician has been putting out some nice articles on natural products that are fair and well-balanced. Here we see further support for the use of saw palmetto for prostate enlargement. I would add to this mix lycopene (the red carotenoid that gives tomatos and watermelo their color) and cruciferous veggies (see below…) for further prostate health.
Saw Palmetto for Prostate Disorders – March 15, 2003 – American Family Physician. Click here for more information.
2-Methoxyestradiol, a Promising Anticancer Agent.
It is very interesting that researchers are viewing this compound as a potential anti cancer compound. Past issues of the Updates have reviewed the concept that estrogens are broken down by several pathways in the body, primary of which are the 16-, 4- and 2-hydroxyestradiol. The 16 pathway is well demonstrated to be genotoxic while the 2 pathway is protective. The 2/16 ratio (which is easily checked in urine or serum) has been linked with several types of cancer, including prostate, breast, endometrial and throat. The wonderful thing about this ratio is that it is modifyable by indole-3-carbinol in cruciferous veggies (unless of course you are on acid-suppressive therapy because stomach acid is needed to activate the compound from foods).
Pharmacotherapy 23(2):165-172, 2003 – Click here for more information.
Estrogens occurring naturally in the body are metabolized to catecholestrogens (2- and 4-hydroxyestradiol) by the cytochrome P450 enzymes. 2-Hydroxy catecholestrogens are further metabolized by catechol-O-methyltransferase to 2-methoxyestradiol, which is known to be protective against tumor formation. 2-Methoxyestradiol exhibits potent apoptotic activity against rapidly growing tumor cells. It also possesses antiangiogenic activity through a direct apoptotic effect on endothelial cells. Other molecular mechanisms, including microtubule stabilization by inhibition of the colchicine-binding site, have been reported. The exact mechanism of action of 2-methoxyestradiol is still unclear, but it has been shown to be effective in preventing tumor growth in a variety of cell lines. 2-Methoxyestradiol also possesses cardioprotective activity by inhibiting vascular smooth muscle cell growth in arteries. It has a lower binding affinity for estrogen receptor alpha compared with that of estradiol, and its affinity for estrogen receptor-beta is even lower than that of estrogen receptor alpha, thus it has minimal estrogenic activity. 2-Methoxyestradiol is distinct because of its inability to engage estrogen receptors as an agonist, and its unique antiproliferative and apoptotic activities are mediated independently of estrogen receptors alpha and beta. A phase I clinical trial of 2-methoxyestradiol 200, 400, 600, 800, and 1000 mg/day in 15 patients with breast cancer showed significant reduction in bone pain and analgesic intake in some patients, with no significant adverse effects. Another phase I study of 2-methoxyestradiol 200-1000 mg/day in combination with docetaxel 35 mg/m2/week for 4-6 weeks performed in 15 patients with advanced refractory metastatic breast cancer showed no serious drug-related adverse effects. A phase II randomized, double-blind trial of 2-methoxyestradiol 400 and 1200 mg/day in 33 patients with hormone-refractory prostate cancer showed that it was well tolerated and showed prostate specific antigen stabilizations and declines. We have started a phase I clinical trial to explore dosages greater than 1000 mg/day.
Nutrition in Crohn Disease-Butyrate.
Butyrate is a short chain fatty acid produces when healthy bacterial flora digest soluble fiber. Butyrate has long been shown to be effective with many GI disorders because it is the preferred fuel source for the cells lining the colon.
Click here for more information
Butyrate is a short-chain fatty acid produced by bacterial fermentation of dietary fiber and undigested starch in the colon. It is important in maintaining the health and integrity of colonic mucosa, as it provides greater than 70% of the energy supply of the colonocyte. Recently, it was demonstrated that butyrate inhibits the inflammatory response in CD by inhibiting the transcription factor nuclear factor kappa B (NFkappaB) activation in immune cells. NFkappaB is involved in inflammatory and immune responses and regulates TNF. By inhibiting NFkappaB, TNF is downregulated and, theoretically, inflammation will be reduced. Already demonstrated in patients with steroid-resistant CD is marked improvement in those patients treated with monoclonal antibodies to TNF. Although further studies are needed to determine the best method of administering butyrate, it offers promise for an immune modulatory therapy for treating patients with CD. Of note, an oral precursor of butyrate has recently been used in ulcerative colitis and was successful in lowering corticosteroid dose. Further utility in CD might be of special interest.