A really decent collection of the multitude of studies that validate the superiority of restricting carbohydrates in human diets...lower bodyfat, improved lipids, reduced inflammation and CVD markers, better bone health and reduced cancer growth among other things...what's not to like?

(edit = typos fixed)

this link does not collect low fat research , and does not it collects low carb research showing inefficacy.

I have no idea what your first sentence means but I find the science demonstrated by this collection compelling. Study after study showing improved health from reducing dietary carbohydrates in humans...

My biggest issue with low carb is the purported difficulty in gaining mass, which I need help with dearly.

Now, does muscle glycogen promote hypertrophy per se or is it just that depletion of liver glycogen and low leptin from lack of dietary carbs / hexosamines stifles the anabolic hormonal environment? Because if that were the case, fructose is not insulinogenic. Although hepatic gluconeogenesis would disrupt ketosis (I assume), you seem to be suggesting that insulin is the bad guy here. If one could signal the fed state w/o glucose, might potential for mass gains be preserved?

So fructose replaces liver glycogen and hexosamines, but isn't as good as glucose in providing higher leptin?

Enough calories = fed state signaling.

And I think we should define our terms here, as "low carb" means different things to different people/different sources. One of the current "low carb gurus" Jeff Volek says, "any diet nominally less than that, say < 35-40%, be considered a 'low-carbohydrate diet.'"

As much as I dislike Polquin, I seem to recall him saying that his athletes don't get anymore than 250g/day (I'll find this if someone wants to read further).

Perhaps the best approach for keeping the benefits of "low carb" and gaining mass would be a very Berardi-like approach of:
1. Eating mostly paleo (meats, nuts, fats, fruits, veggies). You're not going to eat 9 apples in one sitting, so you end up keeping carbs somewhat low, especially if you have enough fat to blunt appetite.
2. Proper Pre/Post workout nutrition, even allowing for 1 more "carb" meal after the PWO shake on workout days.
3. Follow the 10 percent rule, or just have a refeed day once a week.

Insulin is kept under control but carbs are used when needed or "earned."

There's no reason a low carb diet need be ketogenic. Ketosis is protein sparing, but protein is even more protein sparing.

If gaining mass is the goal, as many carbs as one's metabolism can tolerate is probably best.

Low carb comes to the Heartland

My folks sent me an article from the Praire Farmer magazine today. "Study debunks beef's bad rap" detailed the research of Steven Smith at Texas A&M. Nothing revolutionary, but it was interesting to see how low-carb diets are reaching diverse segments of the public.

That's because its posted to demonstrate the superiority of low carb diets over high carb diets (and sometimes low fat diets) in humans.

You should feel free to post links to studies demonstrating the superiority of low fat diets over low-carb diets for improving disease markers, body composition, etc.

And Dash, strategic and short term use of simple carbs insulinogenic effect to assist in bulking seems perfectly reasonable to me. I just think its very clear that it is healthier overall to restrict carbohydrate consumption.

I had heard a while back about how the Ornish Diet was supposed to be excellent for reducing cardiovascular disease risk factors, and that it had been backed by some studies, so I went ahead and did some PubMed searching..


J Am Diet Assoc. 2007 Oct;107(10):1786-91.Click here to read Links

A dietary quality comparison of popular weight-loss plans.
Ma Y, Pagoto SL, Griffith JA, Merriam PA, Ockene IS, Hafner AR, Olendzki BC.

Division of Preventive and Behavioral Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA. Yunsheng.Ma@umassmed.edu

Popular weight-loss plans often have conflicting recommendations, which makes it difficult to determine the most healthful approach to weight loss. Our study compares the dietary quality of popular weight-loss plans. Dietary quality, measured by the Alternate Healthy Eating Index (AHEI), was calculated via sample menus provided in published media for the New Glucose Revolution, Weight Watchers, Atkins, South Beach, Zone, Ornish, and 2005 US Department of Agriculture Food Guide Pyramid (2005 Food Guide Pyramid) plans. The criterion for determining which weight-loss plans were the most popular was their status on the New York Times Bestseller list. Weight Watchers and the 2005 Food Guide Pyramid plan were included because they are the largest commercial weight-loss plan, and the current government recommendation, respectively. Analysis of variance was used to compare nutrient information among the weight-loss plans. The AHEI scores adjusted for energy content were also compared. Of a maximum possible score of 70, the AHEI scores for each weight-loss plan from the highest to the lowest plan were: Ornish (score 64.6), Weight Watchers high-carbohydrate (score 57.4), New Glucose Revolution (score 57.2), South Beach/Phase 2 (score 50.7), Zone (score 49.8), 2005 Food Guide Pyramid (score 48.7), Weight Watchers high-protein (score 47.3), Atkins/100-g carbohydrate (score 46), South Beach/Phase 3 (score 45.6), and Atkins/45-g carbohydrate (score 42.3). Dietary quality varied across popular weight-loss plans. Ornish, Weight Watchers high-carbohydrate, and New Glucose Revolution weight-loss plans have an increased capacity for cardiovascular disease prevention when assessed by the AHEI.

PMID: 17904938 [PubMed - indexed for MEDLINE]



Here's JAMA saying that Low Carb = Low Fat for heart disease and weight loss:

JAMA. 2005 Jan 5;293(1):43-53.

Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial.
Dansinger ML, Gleason JA, Griffith JL, Selker HP, Schaefer EJ.

Division of Endocrinology, Diabetes, and Metabolism, Atherosclerosis Research Laboratory, Tufts-New England Medical Center, Boston, Mass 02111, USA. mdansinger@tufts-nemc.org

CONTEXT: The scarcity of data addressing the health effects of popular diets is an important public health concern, especially since patients and physicians are interested in using popular diets as individualized eating strategies for disease prevention. OBJECTIVE: To assess adherence rates and the effectiveness of 4 popular diets (Atkins, Zone, Weight Watchers, and Ornish) for weight loss and cardiac risk factor reduction. DESIGN, SETTING, AND PARTICIPANTS: A single-center randomized trial at an academic medical center in Boston, Mass, of overweight or obese (body mass index: mean, 35; range, 27-42) adults aged 22 to 72 years with known hypertension, dyslipidemia, or fasting hyperglycemia. Participants were enrolled starting July 18, 2000, and randomized to 4 popular diet groups until January 24, 2002. INTERVENTION: A total of 160 participants were randomly assigned to either Atkins (carbohydrate restriction, n=40), Zone (macronutrient balance, n=40), Weight Watchers (calorie restriction, n=40), or Ornish (fat restriction, n=40) diet groups. After 2 months of maximum effort, participants selected their own levels of dietary adherence. MAIN OUTCOME MEASURES: One-year changes in baseline weight and cardiac risk factors, and self-selected dietary adherence rates per self-report. RESULTS: Assuming no change from baseline for participants who discontinued the study, mean (SD) weight loss at 1 year was 2.1 (4.8) kg for Atkins (21 [53%] of 40 participants completed, P = .009), 3.2 (6.0) kg for Zone (26 [65%] of 40 completed, P = .002), 3.0 (4.9) kg for Weight Watchers (26 [65%] of 40 completed, P < .001), and 3.3 (7.3) kg for Ornish (20 [50%] of 40 completed, P = .007). Greater effects were observed in study completers. Each diet significantly reduced the low-density lipoprotein/high-density lipoprotein (HDL) cholesterol ratio by approximately 10% (all P<.05), with no significant effects on blood pressure or glucose at 1 year. Amount of weight loss was associated with self-reported dietary adherence level (r = 0.60; P<.001) but not with diet type (r = 0.07; P = .40). For each diet, decreasing levels of total/HDL cholesterol, C-reactive protein, and insulin were significantly associated with weight loss (mean r = 0.36, 0.37, and 0.39, respectively) with no significant difference between diets (P = .48, P = .57, P = .31, respectively). CONCLUSIONS: Each popular diet modestly reduced body weight and several cardiac risk factors at 1 year. Overall dietary adherence rates were low, although increased adherence was associated with greater weight loss and cardiac risk factor reductions for each diet group.

PMID: 15632335 [PubMed - indexed for MEDLINE]

I haven't bothered yet to do a search on low-fat diets, instead of just Ornish.

You must have missed this one

Comparison of the Atkins, Zone, Ornish, and LEARN Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women
The A TO Z Weight Loss Study: A Randomized Trial

Christopher D. Gardner, PhD; Alexandre Kiazand, MD; Sofiya Alhassan, PhD; Soowon Kim, PhD; Randall S. Stafford, MD, PhD; Raymond R. Balise, PhD; Helena C. Kraemer, PhD; Abby C. King, PhD

JAMA. 2007;297:969-977.

Context Popular diets, particularly those low in carbohydrates, have challenged current recommendations advising a low-fat, high-carbohydrate diet for weight loss. Potential benefits and risks have not been tested adequately.

Objective To compare 4 weight-loss diets representing a spectrum of low to high carbohydrate intake for effects on weight loss and related metabolic variables.

Design, Setting, and Participants Twelve-month randomized trial conducted in the United States from February 2003 to October 2005 among 311 free-living, overweight/obese (body mass index, 27-40) nondiabetic, premenopausal women.

Intervention Participants were randomly assigned to follow the Atkins (n = 77), Zone (n = 79), LEARN (n = 79), or Ornish (n = 76) diets and received weekly instruction for 2 months, then an additional 10-month follow-up.

Main Outcome Measures Weight loss at 12 months was the primary outcome. Secondary outcomes included lipid profile (low-density lipoprotein, high-density lipoprotein, and non–high-density lipoprotein cholesterol, and triglyceride levels), percentage of body fat, waist-hip ratio, fasting insulin and glucose levels, and blood pressure. Outcomes were assessed at months 0, 2, 6, and 12. The Tukey studentized range test was used to adjust for multiple testing.

Results Weight loss was greater for women in the Atkins diet group compared with the other diet groups at 12 months, and mean 12-month weight loss was significantly different between the Atkins and Zone diets (P<.05). Mean 12-month weight loss was as follows: Atkins, –4.7 kg (95% confidence interval [CI], –6.3 to –3.1 kg), Zone, –1.6 kg (95% CI, –2.8 to –0.4 kg), LEARN, –2.6 kg (–3.8 to –1.3 kg), and Ornish, –2.2 kg (–3.6 to –0.8 kg). Weight loss was not statistically different among the Zone, LEARN, and Ornish groups. At 12 months, secondary outcomes for the Atkins group were comparable with or more favorable than the other diet groups.

Conclusions In this study, premenopausal overweight and obese women assigned to follow the Atkins diet, which had the lowest carbohydrate intake, lost more weight and experienced more favorable overall metabolic effects at 12 months than women assigned to follow the Zone, Ornish, or LEARN diets. While questions remain about long-term effects and mechanisms, a low-carbohydrate, high-protein, high-fat diet may be considered a feasible alternative recommendation for weight loss.


This one doesn't mention Ornish by name but does put a low-carb diet head to head with one that generally follows the low fat recommendations of that diet.


A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia
A Randomized, Controlled Trial
right arrow William S. Yancy, Jr., MD, MHS; Maren K. Olsen, PhD; John R. Guyton, MD; Ronna P. Bakst, RD; and Eric C. Westman, MD, MHS

18 May 2004 | Volume 140 Issue 10 | Pages 769-777

Background: Low-carbohydrate diets remain popular despite a paucity of scientific evidence on their effectiveness.
Objective: To compare the effects of a low-carbohydrate, ketogenic diet program with those of a low-fat, low-cholesterol, reduced-calorie diet.
Design: Randomized, controlled trial.
Setting: Outpatient research clinic.
Participants: 120 overweight, hyperlipidemic volunteers from the community.

Intervention: Low-carbohydrate diet (initially, <20 g of carbohydrate daily) plus nutritional supplementation, exercise recommendation, and group meetings, or low-fat diet (<30% energy from fat, <300 mg of cholesterol daily, and deficit of 500 to 1000 kcal/d) plus exercise recommendation and group meetings.

Measurements: Body weight, body composition, fasting serum lipid levels, and tolerability.

Results: A greater proportion of the low-carbohydrate diet group than the low-fat diet group completed the study (76% vs. 57%; P = 0.02). At 24 weeks, weight loss was greater in the low-carbohydrate diet group than in the low-fat diet group (mean change, 12.9% vs. 6.7%; P < 0.001). Patients in both groups lost substantially more fat mass (change, 9.4 kg with the low-carbohydrate diet vs. 4.8 kg with the low-fat diet) than fat-free mass (change, 3.3 kg vs. 2.4 kg, respectively). Compared with recipients of the low-fat diet, recipients of the low-carbohydrate diet had greater decreases in serum triglyceride levels (change, 0.84 mmol/L vs. 0.31 mmol/L [74.2 mg/dL vs. 27.9 mg/dL]; P = 0.004) and greater increases in high-density lipoprotein cholesterol levels (0.14 mmol/L vs. 0.04 mmol/L [5.5 mg/dL vs. 1.6 mg/dL]; P < 0.001). Changes in low-density lipoprotein cholesterol level did not differ statistically (0.04 mmol/L [1.6 mg/dL] with the low-carbohydrate diet and 0.19 mmol/L [7.4 mg/dL] with the low-fat diet; P = 0.2). Minor adverse effects were more frequent in the low-carbohydrate diet group.

Conclusions: Compared with a low-fat diet, a low-carbohydrate diet program had better participant retention and greater weight loss. During active weight loss, serum triglyceride levels decreased more and high-density lipoprotein cholesterol level increased more with the low-carbohydrate diet than with the low-fat diet.

I saw it, but didn't follow the link because I was looking for generalized studies. Good catch, though.

Because you cannot feed someone a placebo diet, in almost every case, these diet studies pitch a low carb diet against a control diet that is not low carb...sometimes against low fat as well depending on the study goals. And from the research I have done, there are very few studies, if any, that show low carb diets to be ineffective at either reducing body fat, inflammation, etc...there are a few that show what is claimed to be a negative shift in cholesterol but given the lack of convincing evidence tying cholesterol levels to much of anything, I am unconvinced.

I cannot imagine how miserable I would be on the Ornish diet...no meat, fish or nuts, less than 10% of total calories from fat, 20% from protein and a whopping 70% of total caloric intake from carbs...

Liver glycogen: yes, much better than glucose. Hexosamines: don't know. Leptin: don't know.



You sure?

Full text -- not sure about diets being isocaloric here...

Effects of a low-fat versus a low-carbohydrate diet on adipocytokines in obese adults.
de Luis DA, Aller R, Izaola O, Gonzalez Sagrado M, Bellioo D, Conde R.

Institute of Endocrinology and Nutrition, Medical School and Unit of Investigation, Hospital Rio Hortega, University of Valladolid, Valladolid, Spain. dadluis@yahoo.es

BACKGROUND AND AIMS: There are few studies addressing the effect of weight loss on circulating levels of adipocytokines. The aim of our study was to determine whether different diets would have different weight loss effects and to examine the changes in adipocytokine levels. METHODS: A population of 90 obesity non-diabetic outpatients was analyzed in a prospective way. The patients were randomly allocated to two groups: (a) diet I (low-fat diet), and ( diet II (low-carbohydrate diet). At baseline and after 3 months on the diet, adipocytokines were evaluated. RESULTS: 43 patients were randomized to group I and 47 patients to diet group II. No differences were detected between weight loss in either group (3.3 +/- 0.51 vs. 4.4 +/- 0.6 kg; n.s.). In group I, a significant decrease in leptin levels was found. In group II, leptin and C-reactive protein (CRP) levels also decreased. The decrease in leptin levels was lower with diet I than II (16.4 vs. 22.8%; p < 0.05). CONCLUSION: The serum leptin concentration decreased due to the 3-month intervention with low-fat and low-carbohydrate diets, without changes in other adipocytokines. The decrease in leptin and CRP levels were higher with a low-carbohydrate diet than a low-fat diet. Copyright 2007 S. Karger AG, Basel.

PMID: 17284923 [PubMed - indexed for MEDLINE]




V V Could this massive increase between 6 and 36 months be from leptin resistance? V V

The effects of a low-carbohydrate versus low-fat diet on adipocytokines in severely obese adults: three-year follow-up of a randomized trial.
Cardillo S, Seshadri P, Iqbal N.

Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, PA, USA.

BACKGROUND: Adipocytokines are associated with insulin resistance and cardiovascular disease and can be modified with weight loss. While we previously demonstrated weight loss and a reduction in leptin in obese adults who followed a low-carbohydrate diet for 6 months, the long-term effects of this diet on adipocytokines are unknown. METHODS: 132 obese adults with a body mass index of > or = 35 kg/m2 were randomized to receive one year of dietary counseling to follow either a low-carbohydrate diet < 30 g/day (LC) or a caloric-restricted diet (reduced by 500 calories/day with < 30% of calories from fat) (LF). Weight, leptin, adiponectin, TNF-alpha, CRP, and insulin were measured at 0, 6, and 36 months (24 months post-counseling). Follow-up data at was collected for 53 participants who returned at 36 months. RESULTS: Mean weight change from baseline was not different between the groups at 36 months. Between 6 and 36 months weight was unchanged for LF, while LC appeared to regain weight [+ 4.84 +/- 35.6 kg (+ 3.0%)]. This difference, however, was not significant (p = 0.08). Leptin was unchanged in LF at both 6 and 36 months. In LC leptin decreased by 8.49 +/- 6.4 ng/mL or 22.7% at 6 months (p < 0.001) and increased by 10.68 +/- 25.2 ng/mL or 41.9% between 6 and 36 months (p = 0.02). There were no differences in insulin, adiponectin, TNF-alpha, or CRP between the groups. CONCLUSIONS: Favorable changes in leptin that accompany weight loss are not sustained in individuals who followed a low-carbohydrate diet for one year. A low-carbohydrate diet had no significant effect on insulin, adiponectin, TNF-alpha, or CRP compared to a low-fat diet at 36 months.

PMID: 16875041 [PubMed - indexed for MEDLINE]



Plasma leptin is influenced by diet composition and exercise.
Koutsari C, Karpe F, Humphreys SM, Frayn KN, Hardman AE.

Human Muscle Metabolism Research Group, School of Sport and Exercise Sciences, Loughborough University, Loughborough, UK. ckoutsari@hua.gr

OBJECTIVE: A low-fat, high-carbohydrate diet (</=30% of total energy intake as fat) in conjunction with moderate intensity physical activity is widely recommended for weight maintenance and reduction. The aim of this study was to assess the effect of adding daily exercise to a short-term high-carbohydrate diet on fasting and postprandial leptin levels. SUBJECTS: Eight healthy, postmenopausal women aged 60+/-4 y (mean+/-s.d.) (body mass index, BMI: 26.4+/-2.3 kg m(-2); predicted maximal oxygen uptake: 29+/-2 ml kg(-1) min(-1)). DESIGN: Plasma responses were studied after subjects consumed the same high-fat, mixed meal on three occasions: after 3 days on a low-carbohydrate diet (35, 50 and 15% energy from carbohydrate, fat and protein, respectively) (Low-CHO); after 3 days on an isoenergetic high-carbohydrate diet (corresponding values 70, 15 and 15%) (High-CHO); and after 3 days on the same high-carbohydrate diet with 60 min of brisk walking daily (High-CHO-Ex). MEASUREMENTS: Fasting and postprandial plasma or serum concentrations of leptin, glucose and insulin. RESULTS: Fasting leptin was significantly higher (P<0.05) after the High-CHO (18.4+/-2.6 ng ml(-1)) (mean+/-s.e.m.) than after both the Low-CHO and the High-CHO-Ex interventions, which did not differ significantly from each other (16.9+/-2.1 and 15.5+/-2.0 ng ml(-1), respectively; P=0.08). Overall (fasted and postprandial states), plasma leptin concentrations were significantly higher after the High-CHO than after the High-CHO-Ex intervention. There was a strong, positive, linear relation between postprandial insulin responses and postprandial leptin concentrations at 6 h. In addition, there was a strong, negative, linear relation between whole-body insulin sensitivity (based on postprandial responses of glucose and insulin) and postprandial leptin concentrations at 6 h. CONCLUSION: Daily moderate intensity exercise, without concomitant changes in body fat mass, suppressed fasting and postprandial circulating leptin concentrations after consumption of a short-term high-carbohydrate diet. As shown in previous studies, insulin appears to be an important modulator of leptinaemia.

PMID: 12861230 [PubMed - indexed for MEDLINE]


High-fat meals reduce 24-h circulating leptin concentrations in women.
Havel PJ, Townsend R, Chaump L, Teff K.

Department of Nutrition, University of California, Davis 95616, USA. pjhavel@ucdavis.edu

Leptin induces weight loss in rodents via its effects on food intake and energy expenditure. High-fat diets induce weight gain, but the mechanism is not well understood. Previous studies have not found an effect of dietary fat content on fasting leptin. There is a nocturnal increase of leptin, however, which is related to insulin responses to meals. We have reported that adipocyte glucose utilization is involved in insulin-induced leptin secretion in vitro. Accordingly, high-fat, low-carbohydrate (HF/LC) meals, which induce smaller insulin and glucose responses, would produce lower leptin concentrations than low-fat, high-carbohydrate (LF/HC) meals. Blood samples were collected every 30-60 min for 24 h from 19 normal-weight (BMI, 24.2 +/- 0.7 kg/m2; percent body fat = 31 +/- 1%) women on 2 days (10 days apart) during which the subjects were randomized to consume three isocaloric 730-kcal meals containing either 60/20 or 20/60% of energy as fat/carbohydrate. Overall insulin and glycemic responses (24-h area under the curve [AUC]) were reduced by 55 and 61%, respectively, on the HF/LC day (P < 0.0001). During LF/HC feeding, there were larger increases of leptin 4-6 h after breakfast (38 +/- 7%, P < 0.001) and lunch (78 +/- 14%, P < 0.001) than after HF/LC meals (both P < 0.02). During LF/HC feeding, leptin increased from a morning baseline of 10.7 +/- 1.6 ng/ml to a nocturnal peak of 21.3 +/- 1.3 ng/ml (change, 10.6 +/- 1.3 ng/ml; percent change, 123 +/- 16%; P < 0.0001). The amplitudes of the nocturnal rise of leptin and the 24-h leptin AUC were 21 +/- 8% (P < 0.005) and 38 +/- 12% (P < 0.0025) larger, respectively, on the LF/HC day. In summary, consumption of HF/LC meals results in lowered 24-h circulating leptin concentrations. This result may be a consequence of decreased adipocyte glucose metabolism. Decreases of 24-h circulating leptin could contribute to the weight gain during consumption of high-fat diets.

PMID: 10334310 [PubMed - indexed for MEDLINE]

I mean, none of these are conclusive but if leptin signaling relies heavily on insulin and glucose response, how can you say that "a calorie is a calorie" WRT low carb diets?

I should have been more specific: your leptin levels aren't at the rock bottom low end of the physiological range if you're consuming adequate calories. I fully understand leptin is mostly tied to carbohydrate intake.

Honestly, I feel equally shitty and deprived on a low carb diet. I'm not doing either one without a really good reason, and will just stick with a varied diet and exercise.

But if I had to pick one, yeah, low carb. They can take my Pittsburgh grilled rare KC strip when they pry it from my cold, greasy, tasty fingers.

I would hazard a guess that the 'higher carb' diets of the people in studies were often a lot higher in carbs than many people's diets on here, even if they're not strictly eating a low-carb or keto style diet. I don't consider myself a low carb eater at the moment, but my diet is far from carb heavy compared to the average high carb diet.

agree with that...

only carbs i eat (except pwo / refeeds) are fruits and veggies - i don't get tired from them, they dont mess me up or make me fat, this seems to work pretty well, but as soon as i start eating starchy stuff, especially processed stuff things are becomming very bad, getting tired, mood swings, sugar cravings, bad digesting etc etc... stuff yourself can be fun on refeeds tough...

and as said, the normal us guy gets probably around 70 % of carbs in, so even a carb intake of 45-50 % would allready be a controlled one...for me a carb intake of about 150g / day (with about 30g fiber) seems to work best

What do you estimate your cho intake to be relative to your BW? 1x? 1.5x?

Most of the time about 1g/lb I would guess. Weekends are higher, all from low GI/high fibre and relatively low cal sources (blueberries, apples, a slice or two of whole grain sourdough bread that's heavy as a brick, kidney beans etc).

I would doubt that type of diet reflects the usual 'high carb' approach to eating.

No, I really don't think it does.

For some people, it takes a lot more adjustment before it becomes comfortable. I am pretty lucky in that, while I love stuff like donuts, chips ahoy cookies, etc...I can also drop CHO from my diet like a bad habit without suffering much in the way of performance consequences.

To follow on with this, for most people an 'all or nothing' approach to CHO seems to prevail.

i.e. for your common person
low carb = fruits, veggies etc, < 20% cal from CHO
on carb = bagel, cereal, muffin, bars etc. with anywhere from 50% - 70% cals from CHO.

There is a nice middle ground somewhere for most people

There is a reason for this. Eating carbs, particularly higher glycemic carbs makes you want to eat more carbs. Depends on the person and their insulin sensitivity but for many.

Perhaps because you realize the mental and physical effects of ketosis and depleted glycogen stores kinda suck

Besides painful joints and good fat loss, I didn't really notice any mental or physical effects while doing 10 weeks of CKD.

I loved CKD, followed up with UD2 and got down to 7.5% BF for the first time ever.. I love low carb eating, diagnosed hypoglycemic at 12 was significantly overweight for majority of life, mentally I feel great. However, as I increase volume, my performance drops and am unable to finish all sets/reps.. So I currently experimenting with a TKD approach, with about 75g carbs before and 25g after workouts. I do 3x/week full body workouts...


I'll keep it updated..

I don't really notice joint pain at all, then again I'm a young buck.

So am I, early 20s.

Increased joint pain would be from just the lack of carbs dehydrating you.. I noticed a slight irritating in my elbows, but supplementing with sodium, potassium and calcium helped a bit..

when the low carb proponent are going to stop giving the reacharound to each other, maybe they'll sit down for a read.

PS I have many more like these showing that fruits rule, saturated fats suck, and anyway it depends on many other factors




saying "low carb" is better is such a gross over-generalization that will never ever be vindicated. better than what? for whom? why don't you drop you stimulants and fiber supplements and try going low carb? hey, the mesiah Taubes said it will work! do it! its all insulin, who cares?

Do we have evidence that low carbing actually does effect joint health? I've never felt any joint pain while being completely void of carbs...


Dash - the problem with leptin vs. low carb diets in these studies is they have no refeeds. Any or all of us know leptin requires that glucose and I will argue in support of it's affinity towards insulin. Sure a consistanty low carbs diet void of any refeeds and set at a consistant calorie deficit is going to make leptin drop significantly. Thus we refeed.

High carbs diets are good for two things - getting muscluar/strong and getting fat.

I've done low carb many times using no appetite suppressants and no fiber supplements. It's not difficult at all. Appetite suppressants for me are really only needed when I'm using a (relatively) lower fat intake.

Fruits are also fine on a low carb diet, provided they're the right kind and you use moderation. Berries in particular are great.

And glucosamine, I would think -- see my comments later on.




I think the majority of us realize that dietary fiber, micronutrient support, and a proper SFAt:PUFA:MUFA ratio, as well as EFAs, will all be critical to optimum health while on a new diet. This is nothing new. Low carb doesn't mean keto -- and I can eat a shitload of veggies and even some fruit while staying below 50 or 100g or whatever you consider "low."



Ha -- I can't even get muscular on high carbs But fat, hell yes.

Interestingly, I think both these issues (joint pain and leptin) are related. Both will be dependent on carbohydrates going through the "hexosamine" pathway (ref: leptin series), where they'll see some F6P -> glucosamine -> NAcGlucosamine action. Cartilage contains large amounts of hyaluronic acid and chondroitin, both of which are glucosamine derivatives, and we already know the leptin -> glucosamine connection.

I have occasional shoulder pain even when high carb (so does my dad -- probably genetic), but when low carb it gets kinda bad. Right now my Lt shoulder is pretty sensitive. Can you say Cissus?

Ditto on carbs making me fat, not muscular (which is why I give myself the skinny-fat name tag)...

I wonder how much of this joint glucosamine is derived from each gram of CHO taken in... Seems like this would be one of the bodies first priorities upon glucose ingestion (replacing depleted stores of joiny glucosamine).... I can't say it is. Research is required... and I'm about to get in one of those moods..

so why did you stop? eh? that's my main point ain't it. if its so superior and bla why do you stop doing it? because it fucks up your nerurochemistry, immune and what not, and suddenly you're sick, lethargic, don't know why, depressed, sick of training and dieting. the measuring stick for all diet is retention of results and ability to do it for a long time.

Show me some evidence that low-carb eating messes with neurochemisty or immune function. The most miserable and unhealthy I have ever been in my adult life was in the early 90s for six months when I was (stupidly, in retrospect) using an ultrastrict, ultra lowfat/high carb diet...

The Inuit and Masai live (or at one point lived) all of their lives on essentially all animal fat and protein diets in some of the harshest environments in the world both in terms of climate for the former and plethora of infectious agents for the latter and are generally healthier than the average American or European.

People bag low-carb diets not because they are unhealthy but because donuts and their kin taste so damned good...

Low carbs are not the same as low carbs. I think what we need to avoid is lots of simple carbs. Sugars are the worst things particularly fructose. Complex carbs are much better. Starches for example are not so bad. Flour is not sugar but breaks down so rapidly into sugar that it's better to avoid eating lots of that. Veggies and fruits should make up the bulk of your diet along with certain grains.

I stopped for the same reason I stopped a high carb, low fat diet. What reason is that? I'm not entirely sure, otherwise I wouldn't fall off the wagon like I do. Comparatively speaking, I feel much better on low carbs, which is why I do it vs. low fat nowadays. I feel sharper mentally, less lethargy, more motivation, etc. And if you want solid evidence vs. anecdotes, there is a year+ long study that showed that people were able to adhere to a low carb diet longer than they were able to adhere to a low fat diet.

I for one do not advocate doing low carb all the time. I like CKD's, or any sort of diet when carbs are taken in <i>at times</i>. I do not also advocate it for everyone, because I do think that some people do better on higher carbs. For me, however, it seems like it's the way to go.

That's terrible logic, man. People come off low carb for a variety of reasons, but I'm willing to be that some of the top ones are 1) tired of the "hassle" of avoiding carbs (esp. at festive events) 2) for lack of easy-to-come-by variety 3) -- for our crowd -- to put on some muscle weight / optimize high intensity exercise.



One topic that does deserve a little love (in my attention) is that if insulin is the keystone upon which this theory is based, why are we so worried with carbs and glycemic issues, when in reality we should look at insulin index? There can be some pretty wide differences between glycemic and insulin responses -- look at milk products. I'm betting that a big reason my last keto diet produced modest (but not impressive) results was that I ate shitload of cheese -- might as well have been eating the carbs.

Bernstein, J., et al, "Depression of Lymphocyte Transformation Following Oral Glucose Ingestion." American Journal of Clinical Nutrition 30(1977): 613.

Ringsdorf, W., Cheraskin, E. and Ramsay R. "Sucrose Neutrophilic Phagocytosis and Resistance to Disease," Dental Survey, 52, No. 12 (1976): 46-48.

Sanchez, A., et al. "Role of Sugars in Human Neutrophilic Phagocytosis," American Journal of Clinical Nutrition 261 (November 1973): 1180-1184.

These referenes are rather old - I could not locate the abstracts.

Sugar: Sweet Suicide

http://findarticles.com/p/articles/mi_m0IS...ly/ai_104259144
http://findarticles.com/p/articles/mi_m0IS..._107201210/pg_1

Beef and fish are worse - what's a keto diet-er to do?

http://www.ajcn.org/cgi/reprint/66/5/1264

The II angle is a good point. Part of it I think is that protein + carbs illicits a much higher insulin response than protein alone or protein + fat, no? This would explain the high II of milk.

Glycemia and insulinemia in healthy subjects after lactoseequivalent
meals of milk and other food proteins: the role of plasma
amino acids and incretins1–3

Mikael Nilsson, Marianne Stenberg, Anders H Frid, Jens J Holst, and Inger ME Björck
ABSTRACT

Background: Milk products deviate from other carbohydratecontaining
foods in that they produce high insulin responses, despite
their low GI. The insulinotropic mechanism of milk has not been
elucidated.

Objective: The objective was to evaluate the effect of common
dietary sources of animal or vegetable proteins on concentrations of
postprandial blood glucose, insulin, amino acids, and incretin hormones
[glucose-dependent insulinotropic polypeptide (GIP) and
glucagon-like peptide 1] in healthy subjects.

Design: Twelve healthy volunteers were served test meals consisting
of reconstituted milk, cheese, whey, cod, and wheat gluten with
equivalent amounts of lactose. An equicarbohydrate load of whitewheat
bread was used as a reference meal.

Results: A correlation was found between postprandial insulin responses
and early increments in plasma amino acids; the strongest
correlations were seen for leucine, valine, lysine, and isoleucine. A
correlation was also obtained between responses of insulin and GIP
concentrations. Reconstituted milk powder and whey had substantially
lower postprandial glucose areas under the curve (AUCs) than
did the bread reference (
62% and
57%, respectively). Whey
meal was accompanied by higher AUCs for insulin (90%) and GIP
(54%).

Conclusions: It can be concluded that food proteins differ in their
capacity to stimulate insulin release, possibly by differently affecting
the early release of incretin hormones and insulinotropic amino
acids. Milk proteins have insulinotropic properties; the whey fraction
contains the predominating insulin secretagogue. AmJ Clin
Nutr 2004;80:1246 –53.

I keto'ed for a little over a year straight. I felt fine. the only reason I stopped was because I wasn't growing. The only "kind" of diet that will EVER work on a long term scale and has the lieniency to produce the right kind of results when you want them is one based off of carb cycling. All you IF'ers out there can eat it.

That's the exact study I was looking for.

Now how does this fit into the "low carb" and taubes angle -- isocaloric portions of beef and white pasta, and -- low and behold -- the insulin AUC for beef is DOUBLE that of the pasta, roughly equivalent to most breakfast cereals and even white rice. Insulin AUC for egg ~= white pasta.

So if Taubes insulin ideas are the way to go, then low carb might not have much to do with it.

Liorrh was right, Liorrh was right! Taubes was ... wrong?

I would say we need to consider insulin levels throughout the day, rather than just after a meal, but the study below shows (Fig 1 and 2) blood glucose and insulin reaching baseline in the same time frame for a white bread and dairy based meal.

Glycemia and insulinemia in healthy subjects after lactose equivalent meals of milk and other food proteins: the role of plasma
amino acids and incretins

(free full-text online)

I would appear if one eats insulinogenic AA's, there's no avoiding an insulin response (duh)

Several amino acids are potent stimulators of insulin release, either when taken as a protein orally or when
infused intravenously (21), and certain amino acids (eg, the branched-chain amino acids) are more insulinogenic than are
others. van Loon et al (36) showed that the insulin response in healthy subjects was positively correlated with plasma leucine,
phenylalanine, and tyrosine when ingested orally in the form of drinks in combination with glucose. Furthermore, it was concluded that protein hydrolysates stimulate insulin secretion to a higher extent than do intact protein because of a more rapid
increase in postprandial plasma amino acid concentrations. In addition, Calbet and MacLean (37) described a close relation
between the insulin response and the increase in plasma amino acid response, especially for leucine, isoleucine, valine, phenylalanine, and arginine. These findings indicate that the postprandial pattern of plasma amino acids may be an important entity for the insulinogenic properties of food proteins

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Just to close, my low-carb diet is no less effective now than it was yesterday, and I really need to cut out and do some homework.

You bring up a lot of good shit, HL.