There are a number of mechanisms by which low-carb diets enhance satiety:

1. Stabilization of blood glucose and insulin levels as a result of reduced carbohydrate intake. This prevents swings in blood sugar and insulin levels that can interfere with the body’s satiety feedback system and trigger hunger[Mayer][Chaput]. This is the most common mechanism, as reduced carbohydrate intakes are obviously an integral feature of low-carbohydrate diets.

2. Increased fat intake. Low-carbohydrate diets frequently, but not always, involve an increase in fat intake. If the low-carb dieter has previously followed a low-fat diet then a switch to low-carb eating may well produce an increase in fat intake. Dietary fat triggers the release of the satiating hormone cholecystokinin (CCK) that acts to prolong feelings of fullness by slowing gastric emptying time.

By the way, you don’t need to be a lard-slurping keto fanatic to enjoy the benefits of fat-induced CCK release. University of California, Davis researchers compared meals containing 20% energy from fat, 17% protein, 63% carbohydrate, with meals containing 38% fat, 17% protein, and 45% carbohydrate[Schneeman]. These meals were further divided into meals containing dairy and non-dairy fat. The results showed greater CCK response to the higher fat meals. Interestingly, meals with dairy fat also produced greater CCK responses than those with non-dairy fats. This and other studies also found that women have a greater response CCK response to fat ingestion than men, and that the satiating effects of CCK are enhanced by stomach distension[Burton-Freeman][ Melton][Kissileff].

It should be pointed out that while CCK release is usually associated with increased fat intake, at least one study has found an increase in CCK levels on a low-carbohydrate (South Beach) diet during which fat intake actually declined (no overall change was recorded in protein intake, the greatest change was in carbohydrate intake). This study, however, was a free-living endeavour that relied upon self-reported intakes, so the true accuracy and significance of these findings is unknown[Hayes].

A far more controlled study indicated that protein may also have an effect on CCK. This study involved the consumption of both high-protein/low-carb and low-protein/high-carb breakfasts. Despite similar fat intakes, the high protein meal produced a significantly greater increase in CCK levels. The high protein breakfast also reduced appetite and caloric intake during the following lunch meal by 105 calories, but the difference was not statistically significant[Blom].

3. Increased protein intake. Low-carbohydrate diets sometimes, but not always, involve an increase in protein intake. If the low-carb dieter was previously following a low-protein diet (as recommended by some low-fat and vegetarian promoters) then a switch to a low-carb diet may involve an increase in high-protein animal products such as meat, dairy and eggs. The satiating effects of protein have been repeatedly demonstrated in clinical studies[Astrup][Halton].

April 21, 2010 (Atlanta, Georgia) — It's been clear enough that a high-fat diet can worsen serum lipids, but less so that a diet with a lot of added sugar may do it as well. The case for it is stronger with a cross-sectional look at >6000 US adults that found significant, independent associations between increased intake of sugar-sweetened foods, which typically have added sucrose or high-fructose corn syrup, and elevated triglycerides (TG) and reduced HDL-cholesterol levels [1].

The analysis, based on 1999–2006 data from a National Health and Nutrition Examination Survey (NHANES) population, also suggested a big jump in consumption of added sugar compared with NHANES data from almost 30 years earlier, from 10.6% to 15.8% of daily calories, report its authors, led by Jean A Welsh (Emory University, Atlanta, GA), in the April 21, 2010 issue of the Journal of the American Medical Association.

The dyslipidemia findings echo those from the Framingham Heart Study three years ago that associated elevated TG and low HDL-C, among other markers of the metabolic syndrome, with consumption of at least one sweetened soft drink daily [2]. However, in that study, as reported by heartwire at the time, high intake of soft drinks worsened lipids regardless of whether they contained sugar or artificial sweeteners.

But the NHANES analysis is also consistent with a body of literature linking high-carbohydrate diets with elevated risk of stroke and heart-disease events, prospective short-term studies suggesting that increased sugar consumption promotes dyslipidemia, and the well-recognized worsening effects of greater carbohydrate intake on TG and HDL-C levels, senior author Dr Miriam B Vos (Emory University) told heartwire .

The current study, she said, is noteworthy for extending those prospective observations "to a nationally representative free-living population, people consuming their normal diets." It may also be the first of its kind to associate cardiovascular risk factors with dietary added sugars, which may be a more easily modifiable source of calories than simply "sugar" or "carbohydrates," which take many forms naturally in whole foods, according to Vos.

She proposes that a public-health message to cut back on added sugars, which could be easily identified on food labels, may also be easier to understand and accomplish than a recommendation to reduce sugar in general.

The NHANES sample consisted of 3088 nonpregnant women and 3025 men who didn't have "extremely high" triglyceride levels. Diabetics had also been excluded from the cohort, Vos said, "because we felt they would have been given advice that would have substantially changed their diet." Data on sugar intake was collected by interviewer-assisted 24-hour dietary recall.

Persons consuming the most added sugar showed significantly increased adjusted risks of having low HDL-C (<40 mg/dL for men; <50 mg/dL for women) and high TG (>150 mg/dL) according to National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) definitions, compared with those consuming the least. And the likelihoods of having low HDL-C and high TG went up with increasing intake levels (p<0.05 for both trends).

Odds Ratioa for Dyslipidemia Indicatorb by % Total Energy From Added Sugar in NHANES Analysis

Indicator 5% to <10%, (n=893) 10% to <17.5% (n=1751) 17.5% to <25% (n=1210) >25% (n=1135)
Low HDL-C 1.0 (0.8–1.4) 1.5 (1.2–1.9) 1.9 (1.5–2.6) 3.1 (2.3–4.3)c
High triglycerides 0.8 (0.7–1.1) 1.1 (0.9–1.4) 1.3 (1.0–1.6) 1.2 (0.9–1.6)c
High LDL-C 0.9 (0.7–1.2) 1.1 (0.9–1.3) 1.1 (0.9–1.5) 1.2 (0.9–1.7)


a. OR (95% CI) vs reference group (<5% energy from added sugar, n=593); adjusted for age; sex; race/ethnicity; poverty; body-mass index; waist circumference; weight change; physical activity; total energy intake; intake of monounsaturated fatty acids, polyunsaturated fatty acids, saturated fatty acids, cholesterol, fiber, and other carbohydrates; hypertension; cigarette smoking; and alcohol use

b. low and high levels as defined by NCEP-ATP III guidelines

c. p<0.05 for trend

Neither finding was true for high LDL-C levels, which appeared unaffected by consumption of added sugar in the population overall. The investigators considered a trend of rising LDL-C with greater sugar intake among women to be of uncertain reliability, as it was only weakly significant (p=0.047) and based on a subgroup analysis, according to Vos.

"Our results support the importance of dietary guidelines that encourage consumers to limit their intake of added sugars," the group concludes, pointing out that the US guidelines caution against excess added sugars without specifying limits on intake and that the government's "Food Guide Pyramid" portrays calories from added sugars as "discretionary" in that they don't satisfy nutritional needs.

"Most discretionary calorie allowances are small, between 100 and 300 calories, especially for individuals who are not physically active," they write. That level is "substantially lower than that currently consumed by adults in the United States."

As heartwire reported last year, the American Heart Association released recommendations for maximum intake of "added sugars," putting "prudent upper limits" on daily intake at 140 kcal for most US men and 100 kcal for most US women, depending on age and activity level [3].

Vos disclosed that she is "author of and receives royalties from a book about childhood obesity" and is partly supported by a career award from the National Institute of Diabetes and Digestive and Kidney Diseases and the Children’s Digestive Health and Nutrition Foundation. The other coauthors had no disclosures.

High intake of added sugars is associated with increased risk for low HDL cholesterol and high triglycerides, according to a JAMA report.


Researchers studied some 6000 adults participating in the National Health and Nutrition Examination Survey (NHANES). Consumption of added sugars (e.g., high-fructose corn syrup and other caloric sweeteners used in prepared foods) was calculated from 24-hour dietary recalls.


In adjusted analyses, the odds of having low HDL cholesterol and high triglycerides rose significantly with increasing intake of added sugars. For example, compared with adults who got less than 5% of their total energy intake from added sugars, those getting 17.5%–25% of their energy from added sugars were about twice as likely to have low HDL levels.


The researchers found no consistent association between added sugars and LDL cholesterol.

A high fat diet inhibits glycosyltransferase= GnT-4a, an enzyme responsible for GLUT 2 function in the pancreas. GnT-4a basically adds a glycan to GLUT 2 in the pancreas to keep this transporter of glucose on the cell surface. If it is inhibited, the GLUT 2 transporter sinks into the cell hence the pancreatic cell can't "see" how much glucose is out there. This leads to reduced insulin output. While a deficiency of insulin can cause diabetes, too much insulin can also be harmful, and has been found to contribute to the pathogenesis of cancer, cardiovascular disease, ovarian diseases, and Alzheimer’s disease. It may be that suppressing insulin production to some degree could be beneficial in such disorders, and that could theoretically be achieved by inhibiting the GnT-4a glycosyltransferase.

A Few 30 Second Sprints As Beneficial As Hour Long Jog Science Daily — Hamilton, ON. June 1, 2005 -- Just six minutes of intense exercise a week could be as effective as an hour of daily moderate activity suggests new findings from researchers at McMaster University. "Short bouts of very intense exercise improved muscle health and performance comparable to several weeks of traditional endurance training," says Martin Gibala, an associate professor in the department of kinesiology of McMaster. The research, which is published in the June edition of the Journal of Applied Physiology, found that performing repeated bouts of high-intensity "sprint"-type exercise resulted in profound changes in skeletal muscle and endurance capacity, similar to training that requires hours of exercise each week. The study was conducted on 16 subjects: eight who performed a two-week sprint interval training program and eight who did no exercise training. The training program consisted of between four and seven 30-second bursts of "all out" cycling followed by four minutes of recovery three times a week for two weeks. Researchers found that endurance capacity in the sprint group increased on average from 26 minutes to 51 minutes, whereas the control group showed no change. The muscles of the trained group also showed a significant increase in citrate synthase, an enzyme that is indicative of the tissue's ability to utilize oxygen. "Sprint training may offer an option for individuals who cite "lack of time" as a major impediment to fitness and conditioning," said Gibala. "This type of training is very demanding and requires a high level of motivation, however less frequent, higher intensity exercise can indeed lead to improvements in health and fitness." ### McMaster University, named Canada's Research University of the Year by Research InfoSource, has world-renowned faculty and state-of-the-art research facilities. McMaster's culture of innovation fosters a commitment to discovery and learning in teaching, research and scholarship. Based in Hamilton, the University has a student population of more than 23,000 and more than 112,000 alumni in 128 countries. Note: This story has been adapted from a news release issued by McMaster University.

How To Burn More Fat, With Less Effort Science Daily — Researchers from the University of New South Wales (UNSW) have found an easier way of getting off those extra kilos you may have gained over the holiday season. The team has trialled a different way of exercising, which burns more fat than regular continuous exercise. “The group which did around eight seconds of sprinting on a bike, followed by 12 seconds of exercising lightly for twenty minutes, lost three times as much fat as other women, who exercised at a continuous, regular pace for 40 minutes,” said the team leader, Associate Professor Steve Boutcher, Head of the Health and Exercise Science program, in the School of Medical Sciences at UNSW. The study involved a group of 45 overweight women who cycled three times a week over a 15-week period. Professor Boutcher said this would be applicable to other types of exercise such as swimming, walking, and rowing. The results have been presented at recent meetings of the Heart Foundation and American College of Sports Medicine. “We think the reason that it works is because it produces a unique metabolic response,” said Professor Boutcher. “Intermittent sprinting produces high levels of chemical compounds called catecholamines, which allow more fat to be burned from under the skin and within the exercising muscles. The resulting increase in fat oxidation drives the greater weight loss.” The women lost most weight off the legs and buttocks. “This maybe unique to this type of exercise,” said Professor Boutcher. “We know it is very difficult to ‘spot reduce’ troublesome fat areas. When you do regular exercise, you tend to lose fat everywhere and you tend to look emaciated. Our results are unusual but were consistent across the women who performed the sprinting exercise.” “Overall, any type of exercise is good. You just have to work out your objectives, whether it is to increase muscle, lose fat, or enhance other aspects of your life such as improving the quality of your sleep,” said Professor Boutcher. And there is a positive message for some people who are overweight. “A lot of people are fat despite having a good diet and a high level of physical activity,” he said. “But being ‘fat and fit’ is much healthier than being lean and unfit. Those overweight people who don’t have excessive fat around their abdomen and don’t have low grade inflammation typically stay healthy and don’t become diabetics. “The message that fat is awful is an exaggerated one,” he said.

Blood sugar comes from 2 places, 1 from food as carbohydrates and 2 from the liver through gluconeogenesis/glycogenolysis. A low carb diet will certainly lower the blood sugar. What about the high morning blood sugar where the sugar comes primarily from the liver (through gluconeogenesis). To deplete this, one would have to lower the sugar (glycogen) in the skeletal muscle (most diabetics have a good supply of skeletal muscle). Since the skeletal muscle burns fuel at 4 rates (phosphagen, lactic acid, glycogen oxidation and fatty acid oxidation), where only 2 of these cycles involve burning sugar ie the lactic acid and glycogen oxidation- note that walking is primarily a fatty acid oxidizing method and would not deplete much sugar from the skeletal muscle-. It is noted that diabetics die primarily of heart dx and the level of exercise to deplete skeletal muscle vs straining cardiac muscle could be tricky. If weight lifting of primarily compound (full body systems ie squats, deadlifts) movements to the extent that next day soreness is experienced=> lactic acid, this should deplete skeletal muscle glycogen ( recall-soreness = lactic acid <- pyruvate <-glucose<- glycogen in the muscle) . The nocturnal glucogenesis now will instead of overfilling the blood, will in fact slowly fill the depleted muscle glycogen stores. This is conjecture based on biological systems and has not been proven in a court of natural law. ...The utility of anaerobic glycolysis, to a muscle cell when it needs large amounts of energy, stems from the fact that the rate of ATP production from glycolysis is approximately 100X faster than from oxidative phosphorylation. During exertion muscle cells do not need to energize aerobic reaction pathways. The requirement is to generate the maximum amount of ATP, for muscle contraction, in the shortest time frame. This is why muscle cells derive almost all of the ATP consumed during exertion from anaerobic glycolysis...indiana state u biochem course-of course the fastest rate of ATP production is the phosphagen cycle but only lasts 6 seconds

Axioms w/c are held to be true but may not be 1) glucose comes either from food or from the liver 2) type 2 diabetes have a high level of glucose in the blood. 3) insulin/glucagon ratio determines the amount of gluconeogenesis in the liver 4) the liver releases glucose either via glycogen breakdown (recall it can store 5% weight of glycogen=> liver weighs 1.2-1.5 kg=>60grams to 75 grams of glycogen, recall any excess glucose to the liver is converted to saturated palmitoyl fa) or gluconeogenesis. 5) Type 2 diabetics have lower stores of glycogen in their liver 6) ethanol slows gluconeogenesis in the liver. 6) glucose downregulates gluconeogenesis in non diabetics but not diabetics. If we were to halt oral glucose, and halt gluconeogenesis at nite with a shot of ethanol, blood glucose levels should fall over time. Weight lifting should also deplete muscle glucose via lactic acid

The faster rxns have less steps but are depleted fastest


The fuels used in anaerobic exercises—sprinting, for example—differ from those used in aerobic exercises—such as distance running. The selection of fuels during these different forms of exercise illustrates many important facets of energy transduction and metabolic integration. ATP directly powers myosin, the protein immediately responsible for converting chemical energy into movement (Chapter 34). However, the amount of ATP in muscle is small. Hence, the power output and, in turn, the velocity of running depend on the rate of ATP production from other fuels. As shown in Table 30.3, creatine phosphate (phosphocreatine) can swiftly transfer its high-potential phosphoryl group to ADP to generate ATP (Section 14.1.5). However, the amount of creatine phosphate, like that of ATP itself, is limited. Creatine phosphate and ATP can power intense muscle contraction for 5 to 6 s. Maximum speed in a sprint can thus be maintained for only 5 to 6 s (see Figure 14.7). Thus, the winner in a 100-meter sprint is the runner who slows down the least.

A 100-meter sprint is powered by stored ATP, creatine phosphate, and anaerobic glycolysis of muscle glycogen. The conversion of muscle glycogen into lactate can generate a good deal more ATP, but the rate is slower than that of phosphoryl-group transfer from creatine phosphate. During a ~10-second sprint, the ATP level in muscle drops from 5.2 to 3.7 mM, and that of creatine phosphate decreases from 9.1 to 2.6 mM. The essential role of anaerobic glycolysis is manifested in the elevation of the blood-lactate level from 1.6 to 8.3 mM. The release of H + from the intensely active muscle concomitantly lowers the blood pH from 7.42 to 7.24. This pace cannot be sustained in a 1000-meter run (~132 s) for two reasons. First, creatine phosphate is consumed within a few seconds. Second, the lactate produced would cause acidosis. Thus, alternative fuel sources are needed.

The complete oxidation of muscle glycogen to CO 2 substantially increases the energy yield, but this aerobic process is a good deal slower than anaerobic glycolysis. However, as the distance of a run increases, aerobic respiration, or oxidative phosphorylation, becomes increasingly important. For instance, part of the ATP consumed in a 1000-meter run must come from oxidative phosphorylation. Because ATP is produced more slowly by oxidative phosphorylation than by glycolysis (see Table 30.3), the pace is necessarily slower than in a 100-meter sprint. The championship velocity for the 1000-meter run is about 7.6 m/s, compared with approximately 10.2 m/s for the 100-meter event (Figure 30.19).

The running of a marathon (26 miles 385 yards, or 42,200 meters), requires a different selection of fuels and is characterized by cooperation between muscle, liver, and adipose tissue. Liver glycogen complements muscle glycogen as an energy store that can be tapped. However, the total body glycogen stores (103 mol of ATP at best) are insufficient to provide the 150 mol of ATP needed for this grueling ~2-hour event. Much larger quantities of ATP can be obtained by the oxidation of fatty acids derived from the breakdown of fat in adipose tissue, but the maximal rate of ATP generation is slower yet than that of glycogen oxidation and is more than tenfold slower than that with creatine phosphate. Thus, ATP is generated much more slowly from high-capacity stores than from limited ones, accounting for the different velocities of anaerobic and aerobic events.

ATP generation from fatty acids is essential for distance running. However, a marathon would take about 6 hours to run if all the ATP came from fatty acid oxidation, because it is much slower than glycogen oxidation. Elite runners consume about equal amounts of glycogen and fatty acids during a marathon to achieve a mean velocity of 5.5 m/s, about half that of a 100-meter sprint. How is an optimal mix of these fuels achieved? A low blood-sugar level leads to a high glucagon/insulin ratio, which in turn mobilizes fatty acids from adipose tissue. Fatty acids readily enter muscle, where they are degraded by β oxidation to acetyl CoA and then to CO 2 . The elevated acetyl CoA level decreases the activity of the pyruvate dehydrogenase complex to block the conversion of pyruvate into acetyl CoA. Hence, fatty acid oxidation decreases the funneling of sugar into the citric acid cycle and oxidative phosphorylation. Glucose is spared so that just enough remains available at the end of the marathon. The simultaneous use of both fuels gives a higher mean velocity than would be attained if glycogen were totally consumed before the start of fatty acid oxidation.

" Now, in the wake of the three Woman’s Health Initiative studies showing that fat doesn’t seem to cause heart disease nor cancers or the breast or colon, comes a study from the venerable NHANES II data showing that not only does salt intake (or to be more precise, sodium intake) not cause premature death from heart disease it actually seems to protect against it. And consuming more sodium appears to protect against premature deaths from not just heart disease but from all other causes as well." Say what? Fat and salt are NOT bad for us? Let's see if I can get agreement. http://www.bmj.com/cgi/content/full/bmj%3b322/7289/757=> "little effect on total mortality" with fat consumption = 95% confidence interval 0.86 to 1.12. and "No statistically significant associations were reported either among Japanese-American men of the Honolulu Heart Study or in the MRFIT cohort." with salt consumption. So WHY does the gov't want to waste my money on these apparently controversial food information? Oh yeah to save me money in the long run for diabetes costs etc even though they don't have a shred of evidence what the causes are. Let's concede for fun, although I don't buy it, that these factors cause diabetes, heart dx etc. and we'll also assume for fun that people will read the nutritional info. and adjust their behavior, I'm friggin sure, then the gov't will have made a wise investment in our tax dollars, right? Alas here comes this from Plos=Fat People Cheaper to Treat. With respect to people who were either obese or thin (smokers were also included and are not costing gov't as much as those damn healthy people) "Cancer incidence, except for lung cancer, was the same in all three groups. Obese people had the most diabetes, and healthy people had the most strokes. Ultimately, the thin and healthy group cost the most, about $417,000, from age 20 on.

The cost of care for obese people was $371,000, and for smokers, about $326,000."

There you go, salt/fat don't make us live shorter and even if they did, it'd end up costing us more anyway

Just last month 2007, the American Heart Association and the American College of Sports Medicine published joint guidelines for physical activity and health. 'It is reasonable to assume that persons with relatively high daily energy expenditures would be less likely to gain weight over time compared with those who have low energy expenditures. So far, data to support this hypothesis is not particularly compelling.' In other words, despite half a century of efforts to prove otherwise, scientists still can't say exercise will help keep the pounds off.

By Howard Wolinsky

NEW YORK (Reuters Health) Apr 01 - A high-protein, low-carbohydrate diet is a safe and effective way for severely obese teenagers to lose weight, according to a new study.

Effective treatment options for young people who are obese are limited, "particularly for those who are severely obese," Dr. Nancy F. Krebs, professor of pediatrics and head of the division of pediatric nutrition at the University of Colorado Denver School of Medicine and colleagues noted online March 22nd in the Journal of Pediatrics.

Fear that a high-protein, low-carbohydrate diet in children "could adversely impact growth and could increase cholesterol levels...has been a barrier to it being used," Dr. Krebs told Reuters Health.

To investigate, the researchers randomized 46 severely obese teenagers to eat either a high-protein, low-carbohydrate diet or a low-fat diet for 13 weeks. The study subjects were 14 years old on average and were at least 175% above ideal weight, but were free of type 2 diabetes and other comorbidities.

On average, those on the high-protein, low-carb diet lost 29 pounds over 13 weeks, while those on the low-fat diet lost 16 pounds. Nine months later, both groups had maintained the weight loss. "We had expected the high-protein, low-carbohydrate group to quickly regain all the weight lost, but this did not occur," Dr. Krebs said. "At the end of the day, this suggests that with ongoing support, these patients could perhaps have achieved even more weight loss."

The high-fat, low-carbohydrate diet also appeared to be safe, with no serious harmful effects on growth, bone mineral density, and various metabolic parameters, such as cholesterol levels. Both groups had declines in LDL cholesterol and increases in HDL cholesterol.

Clinical psychologist Dr. Angela Celio Doyle of the University of Chicago's eating and weight disorders program, who was not involved in the study, said its findings help "fill the hole" in the scientific literature on adolescent obesity.

"There really isn't any gold standard now for how to help these adolescents lose weight," she said.

The study received funding from the National Institutes of Health and the National Cattlemen's Beef Association.

J Pediatr 2010.