Publications by authors named "Loren Cordain"

Purpose Of Review: This review evaluates cow milk's impact on breast carcinogenesis by linking recent epidemiological evidence and new insights into the molecular signaling of milk and its constituents in breast cancer (BCa) pathogenesis.

Recent Findings: Recent prospective cohort studies support the association between cow's milk consumption and the risk of estrogen receptor-α-positive (ER) BCa. Milk is a complex biological fluid that increases systemic insulin-like growth factor 1 (IGF-1), insulin and estrogen signaling, and interacting hormonal promoters of BCa.

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Vegan diets are widely promoted as protective against cardiovascular disease (CVD); however, removing all animal foods from a human's diet usually causes unfavorable health consequences. Our hominin ancestors began consuming meat, fish, seafood, and eggs >2 million years ago. Consequently, humans are genetically adapted to procure nutrients from both plant and animal sources.

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We hypothesize that the major environmental determinant of the expression of essential hypertension in America and other Westernized countries is dietary imprudence in respect of the consumption of daily combinations of foods containing suboptimal amounts of potassium and blood pressure-lowering phytochemicals, and supraphysiological amounts of sodium. We offer as premise that Americans on average consume suboptimal amounts of potassium and blood pressure-lowering phytochemicals, and physiologically excessive amounts of sodium, and that such dietary imprudence leads to essential hypertension through oxidative stress-induced vascular endothelial and smooth muscle dysfunction. Such dysfunctions restrict nitric oxide bioavailability, impairing endothelial cell-mediated relaxation of the underlying vascular smooth muscle, initiating and maintaining inappropriately increased peripheral and renal vascular resistance.

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Milk is rich in miRNAs that appear to play important roles in the postnatal development of all mammals. Currently, two competing hypotheses exist: the functional hypothesis, which proposes that milk miRNAs are transferred to the offspring and exert physiological regulatory functions, and the nutritional hypothesis, which suggests that these molecules do not reach the systemic circulation of the milk recipient, but merely provide nutrition without conferring active regulatory signals to the offspring. The functional hypothesis is based on indirect evidence and requires further investigation.

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The focus of this paper is to explore better strategies for optimising bone strength and reducing risk of fracture, while at the same time decreasing risk of cardiovascular disease. The majority of Americans do not consume the current recommended dietary allowance for calcium, and the lifetime risk of osteoporosis is about 50%. However, traditional mononutrient calcium supplements may not be ideal.

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Milk protein intake has recently been suggested to improve metabolic health. This Perspective provides evidence that metabolic effects of milk protein intake have to be regarded in the context of the individual's pre-existing metabolic and exercise status. Milk proteins provide abundant branched-chain amino acids (BCAAs) and glutamine.

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Prostate cancer (PCa) is dependent on androgen receptor signaling and aberrations of the PI3K-Akt-mTORC1 pathway mediating excessive and sustained growth signaling. The nutrient-sensitive kinase mTORC1 is upregulated in nearly 100% of advanced human PCas. Oncogenic mTORC1 signaling activates key subsets of mRNAs that cooperate in distinct steps of PCa initiation and progression.

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A large proportion of the health woes beleaguering modern cultures are because of daily physical activity patterns that are profoundly different from those for which we are genetically adapted. The ancestral natural environment in which our current genome was forged via natural selection called for a large amount of daily energy expenditure on a variety of physical movements. Our genes that were selected for in this arduous and demanding natural milieu enabled our ancestors to survive and thrive, leading to a very vigorous lifestyle.

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Many of the pervasive health concerns in modern society are the result of diet and lifestyle choices that are at odds with the evolutionary milieu for which we remain genetically adapted. This systematic displacement from a very physically active lifestyle in a natural outdoor environment to a sedentary indoor lifestyle may be at the root of many chronic diseases that are endemic in our culture. A proposed solution is to simulate indigenous human activity patterns in a way that is possible and practical for individuals to achieve.

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Our genome adapts slowly to changing conditions of existence. Many diseases of civilisation result from mismatches between our Paleolithic genome and the rapidly changing environment, including our diet. The objective of the present study was to reconstruct multiple Paleolithic diets to estimate the ranges of nutrient intakes upon which humanity evolved.

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The systematic displacement from a very physically active lifestyle in our natural outdoor environment to a sedentary, indoor lifestyle is at the root of many of the ubiquitous chronic diseases that are endemic in our culture. The intuitive solution is to simulate the indigenous human activity pattern to the extent that this is possible and practically achievable. Suggestions for exercise mode, duration, intensity, and frequency are outlined with a focus on realigning our daily physical activities with the archetype that is encoded within our genome.

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Objective: Better understanding of the relationships between body composition and insulin resistance.

Results: Average human adiposity and sarcopenia have attained unprecedented levels and the resultantly abnormal body composition distorts insulin receptor balance. Compared to evolutionary norms we now have too many adipocyte insulin receptors (in adipose tissue and liver) and too few myocyte insulin receptors.

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A large and growing body of evidence indicates that dietary fatty acids regulate crucial metabolic processes involved in the pathogenesis of coronary heart disease (CHD). Despite this evidence, optimal dietary fatty acid intakes for CHD prevention remain unclear. Significant gaps in the modern nutrition literature and contradictions in its interpretation have precluded broad consensus.

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This editorial outlines the data supporting aggressive lipid goals and options for treating low-density lipoprotein (LDL) cholesterol to a range of approximately 30 to 70 mg/dl. The physiologically normal cholesterol range is approximately 30 to 70 mg/dl for native hunter-gatherers, healthy human neonates, free-living primates, and virtually all wild mammals. Randomized statin trials in patients with recent acute coronary syndromes and stable coronary artery disease have demonstrated that cardiovascular events are reduced and cardiovascular survival optimized when LDL cholesterol is reduced to <70 mg/dl.

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Within the dermatology community, a general consensus has emerged that diet is unrelated to the etiology of acne. Except for 2 poorly designed studies, now more than 30 years old, there are few objective data to support this notion. In contrast, a large body of evidence now exists showing how diet may directly or indirectly influence the following 5 proximate causes of acne: (1) increased proliferation of basal keratinocytes within the pilosebaceous duct, (2) incomplete separation of ductal corneocytes from one another via impairment of apoptosis and subsequent obstruction of the pilosebaceous duct, (3) androgen-mediated increases in sebum production, (4) colonization of the comedo by Propionibacterium acnes, and (5) inflammation both within and adjacent to the comedo.

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In most carbohydrate-containing foods, the blood insulin response is predictable and is closely linked to the food's glycaemic index (GI). A single study, examining whole milk and fermented milk products made from whole milk, recently reported a large dissociation between the GI and insulinaemic index (II) in healthy normal adults. Because the fat component of a food may influence the GI and II, it is unclear if a similar dissociation may exist for skimmed milk in normal adults.

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There is growing awareness that the profound changes in the environment (eg, in diet and other lifestyle conditions) that began with the introduction of agriculture and animal husbandry approximately 10000 y ago occurred too recently on an evolutionary time scale for the human genome to adjust. In conjunction with this discordance between our ancient, genetically determined biology and the nutritional, cultural, and activity patterns of contemporary Western populations, many of the so-called diseases of civilization have emerged. In particular, food staples and food-processing procedures introduced during the Neolithic and Industrial Periods have fundamentally altered 7 crucial nutritional characteristics of ancestral hominin diets: 1) glycemic load, 2) fatty acid composition, 3) macronutrient composition, 4) micronutrient density, 5) acid-base balance, 6) sodium-potassium ratio, and 7) fiber content.

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The normal low-density lipoprotein (LDL) cholesterol range is 50 to 70 mg/dl for native hunter-gatherers, healthy human neonates, free-living primates, and other wild mammals (all of whom do not develop atherosclerosis). Randomized trial data suggest atherosclerosis progression and coronary heart disease events are minimized when LDL is lowered to <70 mg/dl. No major safety concerns have surfaced in studies that lowered LDL to this range of 50 to 70 mg/dl.

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Our genetic make-up, shaped through millions of years of evolution, determines our nutritional and activity needs. Although the human genome has remained primarily unchanged since the agricultural revolution 10,000 years ago, our diet and lifestyle have become progressively more divergent from those of our ancient ancestors. Accumulating evidence suggests that this mismatch between our modern diet and lifestyle and our Paleolithic genome is playing a substantial role in the ongoing epidemics of obesity, hypertension, diabetes, and atherosclerotic cardiovascular disease.

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Compensatory hyperinsulinemia stemming from peripheral insulin resistance is a well-recognized metabolic disturbance that is at the root cause of diseases and maladies of Syndrome X (hypertension, type 2 diabetes, dyslipidemia, coronary artery disease, obesity, abnormal glucose tolerance). Abnormalities of fibrinolysis and hyperuricemia also appear to be members of the cluster of illnesses comprising Syndrome X. Insulin is a well-established growth-promoting hormone, and recent evidence indicates that hyperinsulinemia causes a shift in a number of endocrine pathways that may favor unregulated tissue growth leading to additional illnesses.

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Background: In westernized societies, acne vulgaris is a nearly universal skin disease afflicting 79% to 95% of the adolescent population. In men and women older than 25 years, 40% to 54% have some degree of facial acne, and clinical facial acne persists into middle age in 12% of women and 3% of men. Epidemiological evidence suggests that acne incidence rates are considerably lower in nonwesternized societies.

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