So this guy on a german website (therefore it's german, I'll post it anyway)
claims that being low carb on a long term can be quite dangerous because, so he says, it raises cortisol (because it somehow is needed to convert protein from your muscles into carbs, ketosis isn't enough) and the cortisol messes with your thyroid hormones (t3 and t4). Is there anything about this? I know that too much protein might spike your insulin, but being higher carb and therefore, eating more carbs, also does this.
I'm a little worried. What do you think?
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I think that low carb (VLC) can be done if managed properly, assuming those on it are telling the truth. I went about 6 months, lost weight after breaking a long held plateau but suffered in the constipation department. I found it easier to add back some starches like potatoes, sweet potatoes and a bit of white rice. I do better with 100-150g carbs. I think it best to try it, realize what the potential symptoms are and raise your carbs back up if you have issues.
THE BELOW pretty much says, that low carbohydrate diets may not be as "DEADLY" as people assume! n engl j med 359;3 www.nejm.org july 17, 2008 229 The new england journal of medicine established in 1812 july 17, 2008 vol. 359 no. 3 Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet Iris Shai, R.D., Ph.D., Dan Schwarzfuchs, M.D., Yaakov Henkin, M.D., Danit R. Shahar, R.D., Ph.D., Shula Witkow, R.D., M.P.H., Ilana Greenberg, R.D., M.P.H., Rachel Golan, R.D., M.P.H., Drora Fraser, Ph.D., Arkady Bolotin, Ph.D., Hilel Vardi, M.Sc., Osnat Tangi-Rozental, B.A., Rachel Zuk-Ramot, R.N., Benjamin Sarusi, M.Sc., Dov Brickner, M.D., Ziva Schwartz, M.D., Einat Sheiner, M.D., Rachel Marko, M.Sc., Esther Katorza, M.Sc., Joachim Thiery, M.D., Georg Martin Fiedler, M.D., Matthias Blüher, M.D., Michael Stumvoll, M.D., and Meir J. Stampfer, M.D., Dr.P.H., for the Dietary Intervention Randomized Controlled Trial (DIRECT) Group ABSTRACT Background Trials comparing the effectiveness and safety of weight-loss diets are frequently limited by short follow-up times and high dropout rates. Methods In this 2-year trial, we randomly assigned 322 moderately obese subjects (mean age, 52 years; mean body-mass index [the weight in kilograms divided by the square of the height in meters], 31; male sex, 86%) to one of three diets: low-fat, restricted-calorie; Mediterranean, restricted-calorie; or low-carbohydrate, non–restricted-calorie. Results The rate of adherence to a study diet was 95.4% at 1 year and 84.6% at 2 years. The Mediterranean-diet group consumed the largest amounts of dietary fiber and had the highest ratio of monounsaturated to saturated fat (P<0.05 for all comparisons among treatment groups). The low-carbohydrate group consumed the smallest amount of car bohydrates and the largest amounts of fat, protein, and cholesterol and had the highest percentage of participants with detectable urinary ketones (P<0.05 for all comparisons among treatment groups). The mean weight loss was 2.9 kg for the low-fat group, 4.4 k g for the Mediterranean- diet group, and 4.7 k g for the low- carbohydrate group ( P<0.0 01 for the interaction bet ween diet group and time); among the 272 participants who com pleted the intervention, the mean weight losses were 3.3 kg, 4.6 kg, and 5.5 kg, respectively. The relative reduction in the ratio of total cholesterol to high-density lipoprotein cholesterol was 20% in the low-carbohydrate group and 12% in the low-fat group (P=0.01). Among the 36 subjects with diabetes, changes in fasting plasma glucose an insulin levels were more favorable among t hose assigned to t he Mediterranean diet than among those assigned to the low-fat diet (P<0.001 for the interaction among diabetes and Mediterranean diet and time with respect to fasting glucose levels). Conclusions Mediterranean and low-carbohydrate diets may be effective alternatives to low-fat diets. The more favorable effects on lipids (with the low-carbohydrate diet) and on glycemic control (with the Mediterranean diet) suggest that personal preferences and metabolic considerations might inform individualized tailoring of dietary interventions. (ClinicalTrials.gov number, NCT00160108)
I got trashed thyroid and adrenals because of VLC-ing for 2.5 years (and keto for a few months too). I'm now higher carb & fiber "lite-Paleo" (with rice, potatoes, fermented dairy, soaked legumes allowed). I now eat between 150 gr and 200 gr net carbs, and lots of starches. I'm now feeling better than in VLC.
So everyone's coming to this conclusion. He's right in one aspect. If by low carb, he means the ketogenic level of dieting long-term, that is, deep ketosis. Then, he's probably right that that will induce hypercortesolemia. But the mechanism is a bit different than how he explains it. It works by diminishing your leptin and the lowered level of leptin will increase your cortisol. The mechanism may not be the same for lowered T3 and FT3. In fact, that leptin decrease has immune consequences and that's the new concern that's emerging about these diets. Leptin is a satiety hormone but its more important role is regulating the adaptive immune system. Obese people may have high leptin and that could lead to the development of diabetes and autoimmune diseases. But those with very low levels of leptin, like those in deep ketosis, could also develop immune problems that show up as autoimmune diseases and hemolytic disorders. Dysregulation of leptin, either at high or low levels, have immune consequences.
This hormone-immune axis is tightly wired and disruption of one could affect the other. That could explain some of the disorders that people encounter upon doing long-term ketosis. But low-carbing in the general sense is not a problem. We're talking about a diet with almost no starchy carbs that usually results in gut disbacteriosis.
Here're some articles you might want to consult regarding the hormone-immune axis and the problems that could result. Specifically long-term leptin deprivation could lead to autoimmune and immune disorders.
"[T]here has been increasing evidence that leptin is involved in the pathogenesis of various autoimmune diseases. Leptin has been shown to enhance immune reactions in autoimmune diseases that are commonly associated with inflammatory responses. Both high and low levels of leptin might contribute to autoimmune diseases."
"More important, leptin deficiency increases susceptibility to infectious and inflammatory stimuli and is associated with dysregulation of cytokine production. Leptin deficiency also causes a defect in hematopoiesis. Leptin regulates T cells responses, polarizing Th cells toward a Th1 phenotype."
That's the hypothetical mechanism. And this is the type of result that you often see when someone's been leptin deprived after being in ketosis long-term. I wish I could say this is my first time seeing a blood result like this.