Should we listen to Dr. Mercola and Weston A Price?

Columbo wrote:

abc123 wrote:

400g carbs. Fruit only. Some times I will and dairy.

400g carbs from fruit only? What's that, 15-20 pieces of fruit a day?!?

oirvblp wrote:

abc123 wrote:
It's because typically an ultra low fat diet always decreases pufa and therefore decreases inflammatory auto immune problems.

FWIW, wasn't meaning that. Here is some info what I mean

What I was meaning is biofilm is made up of calcium, magnesium, iron, fat, etc.. Reducing intake of fat will help here in a similar manner as chelating with EDTA (e.g. detoxamin) for biofilm issues.

A quote =

•He uses a McDougall low-fat diet with patients as biofilms have a fat component to them and eating fats, even healthy fats, may add to the problem of biofilms. The Swank MS low-fat diet may also be helpful.

•As you give more fatty acids, you increase the growth rate of the organism by 150 times. Organism likes fat and fat restriction may be a key to recovery. No meat, no cheese, no oils, no avocados, no nuts.

•Dr. Klinghardt suggested that liposomal artemisinin may be helpful here given that these microbes love fats...

•High protein diets are acidic and a disaster for people with Lyme disease. Stay away from fats.

http://www.betterhealthguy.com/joomla/blog/242-a-deep-look-beyond-lyme

mphatesmpb wrote:Where do biofilms form besides the gut and mouth? It seems like any surface that is part of the digestive tract would be easier to rid of biofilms, since dietary approach can be used. But what about the others?

Espio wrote:
OR receded gums right? I'm 27 years old but my gums are so receded that my teeth look as long as a 60 year old!

LOL, it's funny how "natural health" people say grains cause insulin resistance, with no facts at all, all you can say is that "well man has only had agriculture for 5,000 years so our body hasn't evolved for it yet." That is not a fact, evolution is a theory, and archeology has well proven that we agriculture and civilization has been here for hundreds of thousands of years.

Let's look at real facts other than just this evolutionary mumbo-jumbo:

http://www.ajcn.org/content/78/5/965.short

Whole-grain intake and insulin sensitivity: the Insulin Resistance Atherosclerosis Study1,2,3
Angela D Liese, Amy K Roach, Karen C Sparks, Len Marquart, Ralph B D'Agostino Jr and Elizabeth J Mayer-Davis
1 From the Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia (ADL, AKR, KCS, and EJM-D); the Department of Food Science and Nutrition, University of Minnesota, St Paul (LM); General Mills Inc, Minneapolis (LM); and Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC (RBD).
Background: Increased intake of whole-grain foods has been related to a reduced risk of developing diabetes and heart disease. One underlying pathway for this relation may be increased insulin sensitivity.

Objective: We assessed the relation between dietary intake of whole grain-containing foods and insulin sensitivity (SI).

Design: We evaluated data from the Insulin Resistance Atherosclerosis Study (IRAS Exam I, 1992-1994). Usual dietary intakes in 978 middle-aged adults with normal (67%) or impaired (33%) glucose tolerance were ascertained by using an interviewer-administered, validated food-frequency questionnaire. Whole-grain intake (servings per day) was derived from dark breads and high-fiber and cooked cereals. SI was assessed by minimal model analyses of the frequently sampled intravenous-glucose-tolerance test. Fasting insulin was measured by using a radioimmunoassay. We modeled the relation of whole-grain intake to log(SI + 1) and to log(insulin) by using multivariable linear regression.

Results: On average, IRAS participants consumed 0.8 servings of whole grains/d. Whole-grain intake was significantly associated with SI (ß = 0.082, P = 0.0005) and insulin (ß = -0.0646, P = 0.019) after adjustment for demographics, total energy intake and expenditure, smoking, and family history of diabetes. The addition of body mass index and waist circumference attenuated but did not explain the association with SI. The addition of fiber and magnesium resulted in a nonsignificant association that is consistent with the hypothesis that these constituents account for some of the effect of whole grains on SI.

Conclusion: Higher intakes of whole grains were associated with increases in insulin sensitivity.

Espio wrote:Oh I'm sorry the study I posted is not "real evidence." How about this one, go ahead and reach for as many reasons you can to explain away this:

The authors tested the hypothesis that consumption of whole grain is associated with greater insulin sensitivity and lower body mass index (BMI) (weight (kg)/height (m)2) in adolescents and that this association is stronger among the heaviest adolescents. Two 127-item food frequency questionnaires were administered at the mean ages of 13 years (standard deviation 1.2) and 15 years (standard deviation 1.3) to 285 Minnesota adolescents who underwent two euglycemic insulin clamp studies 2 years apart as part of a protocol evaluating the influence of insulin resistance on development of adverse cardiovascular disease risk factors. Intake of whole grain was examined for associations with BMI and insulin sensitivity (measured as milligrams of glucose uptake per kilogram of lean body mass (Mlbm) per minute). After adjustment for age, gender, race, Tanner stage, and energy intake, mean BMI was 23.6 for adolescents consuming less than serving/day of whole-grain foods, 22.6 for –1 servings/day, and 21.9 for more than 1 servings/day (p = 0.05). After adjustment for age, gender, race, Tanner stage, energy intake, BMI, and physical activity, Mlbm was 11.6, 12.3, and 13.2 mg/kg/minute, respectively, in the three whole grain intake groups (p = 0.02). This relation was stronger among adolescents with higher BMIs (p = 0.001). Whole grain intake was associated with greater insulin sensitivity and lower BMI in adolescents, especially among the heaviest persons.



Now, after you reach for a bunch of reasons for why these studies are flawed, why don't YOU provide a study to back up your theory, that whole grains cause insulin resistance. Besides, you are the one making the outlandish theory here, if you ask anyone on the street chances are they will agree that whole grains are good for you. You are the one making the statement that is against the norm, so the burden of proof is on you.

Mercola concludes that over-consumption of carbohydrates in general is the cause of insulin resistance, but I think there might be more to the story. I could be wrong, but I believe that there's something about grains themselves (and not other sources of carbohydrates) which promote insulin resistance.

if you ask anyone on the street chances are they will agree that whole grains are good for you.

Epidemiological evidence suggests that whole grain intake is associated with reduced risk of type 2 diabetes. However, studies of individual whole grains on the prevention of type 2 diabetes are lacking. The objective of the present study was to examine the effect of different whole grains on type 2 diabetes in an animal model of type 2 diabetes, the Goto–Kakisaki (GK) rat. GK rats were fed either a basal diet or a whole grain-containing diet for 5 months. Whole grain diets contained 65 % whole grain flours of wheat, barley, oats or maize. After 2 months of feeding, fasting plasma glucose concentrations were lower in the wheat, barley and oats groups, compared with the basal group, whereas glycated Hb was significantly greater in the wheat group compared with other groups. Feeding of whole barley and maize increased plasma C-peptide concentrations compared with whole wheat at 2 months. There was a trend in the improvement of insulin resistance with a consumption of barley and oats diets at 2 months (P = 0·06) compared with the basal diet. Oxidative stress markers, urinary thiobarbituric acid-reactive substances and 8-isoprostane, did not improve with whole grain intake at 2 months. At 5 months, whole grain diets did not differ from the basal diet in glycaemic control, insulin secretion, oxidative stress and preservation of pancreatic β-cell mass. These results suggest that the consumption of whole grains may offer modest benefit early in the development of type 2 diabetes, but this benefit is lost with further development of the disease.

abc123 wrote:
Espio, I'm drunk right now but that study is still just a correlation and MP's comments are valid. I WILL agree with you that the burden of proof is rightfully on MPhates. I do not think grains CAUSE disease but eliminating them can be very h
helpful once problems have occurred.

tooyoung wrote:

abc123 wrote:
Espio, I'm drunk right now but that study is still just a correlation and MP's comments are valid. I WILL agree with you that the burden of proof is rightfully on MPhates. I do not think grains CAUSE disease but eliminating them can be very h
helpful once problems have occurred.

abc - Do you drink a certain type of alcohol for health reasons? A drink more pro-hair than others?

Among the effects observed in teh small intestine of lectin fed rodents is stirpping away of the mucous coat to expose naked mucosa and overgrowth of the mucosa by abnormal bacteria and protozoa (Banwell et al., 1988). Lectins also cause discharge of histamine from gastric mast cells (Greer and Pusztai, 1985) which stimulates acid secretion. So, the three main pathogenic factors for peptic ulcer, namely acid stimulation, failure of the mucous defense layer and abnormal bacterial proliferation (Helibacter pylori) are all theoretically linked to lectins...The mucus stripping effect of lectins (Freed and Buckley, 1978) also offers an explanation for the anecdotal finding of many allergists that a "stone age diet," which eliminates most starchy foods and therefore most lectins, protects against common upper respiratory viral infections: without lectins in the throat the nasopharyngeal mucus lining would be more effective as a barrier to viruses. Epithelial cells lining the GI tract in vivo, unlike cells in vitro, are constantly exposed to mechanical stress and consequently, frequently suffer plasma membrane disruptions (McNeil and Ito, 1989). However, cell death is not the only outcome of this type of injury: cells are capable of rapidly repairing and thereby surviving plasma membrane disruptions (NcNeil and Kirchhausen, 2005). One key step of the repair mechanism, reviewed by Steinhardt, 2005 is exocytotic. For large disruptions, this exocytotic reaction functions by adding a 'path' of intracellular membrane to plasma membrane surrounding the disruption site.

Therefore, the mechanism of lectin toxicity in vivo could be due to an inhibitory effect on the exocytosis-based constitutive membrane repair and consequent death of wounded gut epithelial cells. It has been found that those lectins that bind strongly to the cell surfaces potently inhibit repair (Miyake et al., 2007). Lectins are therefore toxic when a cell exposed to them experiences plasma membrane disruption. Since mucus secretion is evoked by membrane disruptions in mucus producing GI tract cells (MIyake et al., 2006), it therefore seems likely that lectins also block secretion of this important lubricant. It was found in cell culture studies that a lectin (WGA) potently blocked ionophore-induced mucus secretion...Thus, lectins also inhibit repair of resident gut epithelial cells and additionally, as the study showed, inhibit secretion of mucus by the cell subpopulation (goblet cells) that produces this lubricant. The mechanism of lectin inhibition of membrane repair remains unclear. Exocytosis, which is required for membrane repair (Steinhardt, 2005), is likely targeted by this class of toxin. Previous studies have shown that lectins can inhibit exocytosis (Boehm and Huck, 1998) and it has been shown that, in particular, mucin exocytosis, which is coupled to repair in the cells, is potently inhibited by lectins. MOreover, it has also been found that inhibition of repair is rapid in onset and rapidly reversed by lectin wash off...

It has been shown here that binding of cell surface glycoproteins by lectins interferes with the exocytotic events associated with membrane repair (mucus secretion) and that lectins potently block repair. Therefore, it has been proposed that a second category of disease can also be explained as a failure in the plasma membrane repair mechanism. Lectins, it is hypothesized, are toxic when present in the GI tract based on two, inter-related effects. First, resealing failure occurs within the general population of GI tract cells normally exposed to membrane disrupting levels of mechanical stress, leading to their necrosis. The second lectin-induced effect is exocytotic failure within the subpopulation of GI tract cells that normally secrete mucus, leading to a decrease in protective, lubricating mucus secretion and a consequent increase in the incidence of mechanically-induced membrane disruption events. Because lectins, based on the damage they do to the lining of the GI tract and their hypertrophic effect, have been implicated in, respectively, celiac disease (Weiser and Douglas, 1976) and cancer (Evans et al., 2002), knowledge of this mechanism may have implications beyond a better understanding of food poisoning.

mphatesmpb on Mon Sep 05, 2011 2:42 pm
Here's a discussion of lectins as disease-causing agents:

Dietary Lectins as Disease Causing Toxicants
http://www.pjbs.org/pjnonline/fin1120.pdf

tonyj wrote:

mphatesmpb on Mon Sep 05, 2011 2:42 pm
Here's a discussion of lectins as disease-causing agents:

Dietary Lectins as Disease Causing Toxicants
http://www.pjbs.org/pjnonline/fin1120.pdf

I found this pretty interesting.

p296, 2nd column last sentence:
"...Another suspect lectin disease is rheumatoid arthritis. ..."

Dr. Cristiano at the Columbia University Medical Center discovered that alopecia areata shared the same genes as Type 1 diabetes and RA.

mphatesmpb wrote:Here you go, Espio:
http://jn.nutrition.org/content/137/6/1401.full.pdf

Have a look at table 5...

Diets high in whole-grains worsen metabolic disease with respect to almost every standard metric: fasting blood glucose, fasting insulin, insulin sensitivity, etc.

Refined-grain diets actually produced slight improvements...this pretty much proves that the FDA's recommendations to increase consumption of whole-grain products is completely bogus.

Background: Previous studies comparing low-carbohydrate and
low-fat diets have not included a comprehensive behavioral treat-
ment, resulting in suboptimal weight loss.

Objective: To evaluate the effects of 2-year treatment with a
low-carbohydrate or low-fat diet, each of which was combined
with a comprehensive lifestyle modification program.

Conclusion: Successful weight loss can be achieved with either a
low-fat or low-carbohydrate diet when coupled with behavioral
treatment. A low-carbohydrate diet is associated with favorable
changes in cardiovascular disease risk factors at 2 years.

Espio wrote:

mphatesmpb wrote:Here you go, Espio:


Have a look at table 5...

Diets high in whole-grains worsen metabolic disease with respect to almost every standard metric: fasting blood glucose, fasting insulin, insulin sensitivity, etc.

Refined-grain diets actually produced slight improvements...this pretty much proves that the FDA's recommendations to increase consumption of whole-grain products is completely bogus.

I don't buy it.

1. That study is with a sample size of only 30 people. The two studies I posted had a sample size of 978 for the first study and 285 for the second. This study you are showing us is barely above the standard of being statistically significant.

2. That study is with overweight people who already having issues. Grains may not be for these people, they probably need a stricter diet. Notice the first study i posted, all the people in the samples had healthy insulin sensitivity.

tonyj wrote:Weight and Metabolic Outcomes After 2 Years on a Low-Carbohydrate Versus Low-Fat Diet A randomized Trial.

Background: Previous studies comparing low-carbohydrate and
low-fat diets have not included a comprehensive behavioral treat-
ment, resulting in suboptimal weight loss.

Objective: To evaluate the effects of 2-year treatment with a
low-carbohydrate or low-fat diet, each of which was combined
with a comprehensive lifestyle modification program.

Conclusion: Successful weight loss can be achieved with either a
low-fat or low-carbohydrate diet when coupled with behavioral
treatment. A low-carbohydrate diet is associated with favorable
changes in cardiovascular disease risk factors at 2 years.

Diet-hormone interactions: Protein/carbohydrate ratio alters reciprocally the plasma levels of testosterone and cortisol and their respective binding globulins in man

Karl E. Anderson M.D., William Rosner M.D.*, M. S. Khan Ph.D.*, Maria I. New M.D.**, Songya Pang M.D.**, Paul S. Wissel M.D. and Attallah Kappas M.D.
* The Rockefeller University Hospital, New York, NY, USA
** Columbia University College of Physicians and Surgeons, St. Lukes-Roosevelt Hospital Center, New York, NY, USA
Revised 13 February 1987. Available online 15 November 2002.
Abstract
The aim of this study was to determine if a change in protein/carbohydrate ratio influences plasma steroid hormone concentrations. There is little information about the effects of specific dietary components on steroid hormone metabolism in humans. Testosterone concentrations in seven normal men were consistently higher after ten days on a high carbohydrate diet (468 ± 34 ng/dl, mean ± S.E.) than during a high protein diet (3.71 ± 23 ng/d1, p<0.05) and were accompanied by parallel changes in sex hormone binding globulin (32.5 ± 2.8 nmol/1 vs. 23.4 ± 1.6 nmol/1 respectively, p<0.01). By contrast, cortisol concentrations were consistently lower during the high carbohydrate diet than during the high protein diet (7.74 ± 0.71 μg/d1 vs. 10.6 ± 0.4 μg/d1 respectively, p<0.05), and there were parallel changes in corticosteroid binding globulin concentrations (635 ± 60 nmol/1 vs. 754 ± 31 nmol/1 respectively p<0.05). The diets were equal in total calories and fat. These consistent and reciprocal changes suggest that the ratio of protein to carbohydrate in the human diet is an important regulatory factor for steroid hormone plasma levels and for liver-derived hormone binding proteins.