|Here you go, Michael ...|
Here's a few studies saying somewhat similar things about the big 3 macronutrients (protein, carbs, and fats) ...
Almonds vs complex carbohydrates in a weight reduction program. Int J Obes Relat Metab Disord. 2003 Nov;27(11):1365-72.
OBJECTIVE: To evaluate the effect of an almond-enriched (high monounsaturated fat, MUFA) or complex carbohydrate-enriched (high carbohydrate) formula-based low-calorie diet (LCD) on anthropometric, body composition and metabolic parameters in a weight reduction program.
INTERVENTION: A formula-based LCD enriched with 84 g/day of almonds (almond-LCD; 39% total fat, 25% MUFA and 32% carbohydrate as percent of dietary energy) or self-selected complex carbohydrates (CHO-LCD; 18% total fat, 5% MUFA and 53% carbohydrate as percent of dietary energy) featuring equivalent calories and protein.
RESULTS: LCD supplementation with almonds, in contrast to complex carbohydrates, was associated with greater reductions in weight/BMI (-18 vs -11%), waist circumference (WC) (-14 vs -9%), fat mass (FM) (-30 vs -20%), total body water (-8 vs -1%) and systolic blood pressure (-11 vs 0%), P=0.0001-0.05.
A 62% greater reduction in weight/BMI, 50% greater reduction in WC and 56% greater reduction in FM were observed in the almond-LCD as compared to the CHO-LCD intervention.
Among subjects with type 2 diabetes, diabetes medication reductions were sustained or further reduced in a greater proportion of almond-LCD as compared to CHO-LCD subjects (96 vs 50%, respectively) [correction].
Replacing complex carbohydrates with almonds (something higher in fat) -- helped folks lose body fat (and reversed -- though did not "cure" -- type 2 diabetes).
Trends in intake of energy and macronutrients--United States, 1971-2000. MMWR Morb Mortal Wkly Rep. 2004 Feb 6;53(4):80-2.
During 1971-2000, the prevalence of obesity in the United States increased from 14.5% to 30.9%.
This report summarizes the results of that analysis, which indicate that, during 1971--2000, mean energy intake in kcals increased, mean percentage of kcals from carbohydrate increased, and mean percentage of kcals from total fat and saturated fat decreased.
We've proportionally increased carbohydrate intake -- and decreased fat intake -- and we're now twice as fat as 30 years ago.
Insulin, macronutrient intake, and physical activity: are potential indicators of insulin resistance associated with mortality from breast cancer? Cancer Epidemiol Biomarkers Prev. 2004 Jul;13(7):1163-72.Recap:
Higher dietary protein intake was associated with better survival for all women (relative risk, 0.4; 95% CI, 0.2-0.8, comparing highest to lowest quartile).
An increase in dietary protein was associated with a statistically-significant 60% reduction in mortality in breast cancer patients.
Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. Am J Clin Nutr. 2004 Nov;80(5):1175-84.Recap:
RESULTS: The mean (+/-SD) total fat intake was 25 +/- 6% of energy. In multivariate analyses, a higher saturated fat intake was associated with a smaller decline in mean minimal coronary diameter (P = 0.001) and less progression of coronary stenosis (P = 0.002) during follow-up.
Compared with a 0.22-mm decline in the lowest quartile of intake, there was a 0.10-mm decline in the second quartile (P = 0.002), a 0.07-mm decline in the third quartile (P = 0.002), and no decline in the fourth quartile (P < 0.001); P for trend = 0.001.
This inverse association was more pronounced among women with lower monounsaturated fat (P for interaction = 0.04) and higher carbohydrate (P for interaction = 0.004) intakes and possibly lower total fat intake (P for interaction = 0.09).
Carbohydrate intake was positively associated with atherosclerotic progression (P = 0.001), particularly when the glycemic index was high. Polyunsaturated fat intake was positively associated with progression when replacing other fats (P = 0.04) but not when replacing carbohydrate or protein. Monounsaturated and total fat intakes were not associated with progression.
CONCLUSIONS: In postmenopausal women with relatively low total fat intake, a greater saturated fat intake is associated with less progression of coronary atherosclerosis, whereas carbohydrate intake is associated with a greater progression.
Higher saturated fat (replacing carbohydrates) was associated with a halted atherosclerotic progression.
Effects of protein, monounsaturated fat, and carbohydrate intake on blood pressure and serum lipids: results of the OmniHeart randomized trial. JAMA. 2005 Nov 16;294(19):2455-64.
INTERVENTIONS: A diet rich in carbohydrates; a diet rich in protein, about half from plant sources; and a diet rich in unsaturated fat, predominantly monounsaturated fat.
RESULTS: Blood pressure, low-density lipoprotein cholesterol, and estimated coronary heart disease risk were lower on each diet compared with baseline. Compared with the carbohydrate diet, the protein diet further decreased mean systolic blood pressure by 1.4 mm Hg (P = .002) and by 3.5 mm Hg (P = .006) among those with hypertension and decreased low-density lipoprotein cholesterol by 3.3 mg/dL (0.09 mmol/L; P = .01), high-density lipoprotein cholesterol by 1.3 mg/dL (0.03 mmol/L; P = .02), and triglycerides by 15.7 mg/dL (0.18 mmol/L; P<.001).
Compared with the carbohydrate diet, the unsaturated fat diet decreased systolic blood pressure by 1.3 mm Hg (P = .005) and by 2.9 mm Hg among those with hypertension (P = .02), had no significant effect on low-density lipoprotein cholesterol, increased high-density lipoprotein cholesterol by 1.1 mg/dL (0.03 mmol/L; P = .03), and lowered triglycerides by 9.6 mg/dL (0.11 mmol/L; P = .02).
Compared with the carbohydrate diet, estimated 10-year coronary heart disease risk was lower and similar on the protein and unsaturated fat diets.
CONCLUSION: In the setting of a healthful diet, partial substitution of carbohydrate with either protein or monounsaturated fat can further lower blood pressure, improve lipid levels, and reduce estimated cardiovascular risk.
A diet rich in protein reduces cardiovascular risk.
The metabolic response to a high-protein, low-carbohydrate diet in men with type 2 diabetes mellitus. Metabolism. 2006 Feb;55(2):243-51.Recap:
We recently reported that in subjects with untreated type 2 diabetes mellitus, a 5-week diet of 20:30:50 carbohydrate-protein-fat ratio resulted in a dramatic decrease in 24-hour integrated glucose and total glycohemoglobin compared with a control diet of 55:15:30.
We now present data on other hormones and metabolites considered to be affected by dietary macronutrient changes.
Urinary pH and calcium were unchanged.
The calculated urea production rate accounted for 87% of protein ingested on the control diet, but only 67% on the test diet, suggesting net nitrogen retention on the latter. The lack of negative effects, improved glucose control, and a positive nitrogen balance suggest beneficial effects for subjects with type 2 diabetes mellitus at risk for loss of lean body mass.
For diabetics, 5 weeks on a diet with 30% protein -- as opposed to a diet with 15% protein -- improved glycemic control, spares lean body mass, and had no negative effect on calcium balance.
Effects of variation in protein and carbohydrate intake on body mass and composition during energy restriction: a meta-regression 1. Am J Clin Nutr. 2006 Feb;83(2):260-74.Recap:
A total of 87 studies comprising 165 intervention groups met the inclusion criteria.
RESULTS: After control for energy intake, diets consisting of < or =35-41.4% energy from carbohydrate were associated with a 1.74 kg greater loss of body mass, a 0.69 kg greater loss of fat-free mass, a 1.29% greater loss in percentage body fat, and a 2.05 kg greater loss of fat mass than were diets with a higher percentage of energy from carbohydrate.
In studies that were conducted for >12 wk, these differences increased to 6.56 kg, 1.74 kg, 3.55%, and 5.57 kg, respectively.
Protein intakes of >1.05 g/kg were associated with 0.60 kg additional fat-free mass retention compared with diets with protein intakes < or =1.05 g/kg. In studies conducted for >12 wk, this difference increased to 1.21 kg. No significant effects of protein intake on loss of either body mass or fat mass were observed.
CONCLUSION: Low-carbohydrate, high-protein diets favorably affect body mass and composition independent of energy intake, which in part supports the proposed metabolic advantage of these diets.
Calorie for calorie, lower-carbohydrate diets cause an extra 12+ pounds (5.57kg) of fat loss, over-and-above what higher-carbohydrate reducing diets do. This is called a 'metabolic advantage.'
Diet, evolution and aging--the pathophysiologic effects of the post-agricultural inversion of the potassium-to-sodium and base-to-chloride ratios in the human diet. Eur J Nutr. 2001 Oct;40(5):200-13.
Theoretically, we humans should be better adapted physiologically to the diet our ancestors were exposed to during millions of years of hominid evolution than to the diet we have been eating since the agricultural revolution a mere 10,000 years ago, and since industrialization only 200 years ago.
Among the many health problems resulting from this mismatch between our genetically determined nutritional requirements and our current diet, some might be a consequence in part of the deficiency of potassium alkali salts (K-base), which are amply present in the plant foods that our ancestors ate in abundance, and the exchange of those salts for sodium chloride (NaCl), which has been incorporated copiously into the contemporary diet, which at the same time is meager in K-base-rich plant foods. Deficiency of K-base in the diet increases the net systemic acid load imposed by the diet.
We know that clinically-recognized chronic metabolic acidosis has deleterious effects on the body, including growth retardation in children, decreased muscle and bone mass in adults, and kidney stone formation, and that correction of acidosis can ameliorate those conditions.
Is it possible that a lifetime of eating diets that deliver evolutionarily superphysiologic loads of acid to the body contribute to the decrease in bone and muscle mass, and growth hormone secretion, which occur normally with age? That is, are contemporary humans suffering from the consequences of chronic, diet-induced low-grade systemic metabolic acidosis?
Our group has shown that contemporary net acid-producing diets do indeed characteristically produce a low-grade systemic metabolic acidosis in otherwise healthy adult subjects, and that the degree of acidosis increases with age, in relation to the normally occurring age-related decline in renal functional capacity.
Can we provide dietary guidelines for controlling dietary net acid loads to minimize or eliminate diet-induced and age-amplified chronic low-grade metabolic acidosis and its pathophysiological sequelae. We discuss the use of algorithms to predict the diet net acid and provide nutritionists and clinicians with relatively simple and reliable methods for determining and controlling the net acid load of the diet.
A more difficult question is what level of acidosis is acceptable. We argue that any level of acidosis may be unacceptable from an evolutionarily perspective, and indeed, that a low-grade metabolic alkalosis may be the optimal acid-base state for humans.
Acidity'll get ya'. Here are some of the most acid (+) -- and most alkaline (-) -- foods (per 100 gram portions) ...
Processed cheese ........+28.7
Whole wheat bread........+8.2
Dietary protein: an essential nutrient for bone health. J Am Coll Nutr. 2005 Dec;24(6 Suppl):526S-36S.Recap:
In sharp opposition to experimental and clinical evidence, it has been alleged that proteins, particularly those from animal sources, might be deleterious for bone health by inducing chronic metabolic acidosis which in turn would be responsible for increased calciuria and accelerated mineral dissolution.
This claim is based on an hypothesis that artificially assembles various notions, including in vitro observations on the physical-chemical property of apatite crystal, short term human studies on the calciuric response to increased protein intakes, as well as retrospective inter-ethnic comparisons on the prevalence of hip fractures.
The main purpose of this review is to analyze the evidence that refutes a relation of causality between the elements of this putative patho-physiological "cascade" that purports that animal proteins are causally associated with an increased incidence of osteoporotic fractures. In contrast, many experimental and clinical published data concur to indicate that low protein intake negatively affects bone health.
In agreement with both experimental and clinical intervention studies, large prospective epidemiologic observations indicate that relatively high protein intakes, including those from animal sources are associated with increased bone mineral mass and reduced incidence of osteoporotic fractures.
As to the increased calciuria that can be observed in response to an augmentation in either animal or vegetal proteins it can be explained by a stimulation of the intestinal calcium absorption. Dietary proteins also enhance IGF-1, a factor that exerts positive activity on skeletal development and bone formation.
Consequently, dietary proteins are as essential as calcium and vitamin D for bone health and osteoporosis prevention. Furthermore, there is no consistent evidence for superiority of vegetal over animal proteins on calcium metabolism, bone loss prevention and risk reduction of fragility fractures.
Higher protein diets are good for bones.