Rethinking Cholesterol and Saturated Fats in the Diet

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One of the top researchers in the world today is a guy who I have known since 1995, Jeff Volek, Ph.D., R.D. He is one of the leading experts in lipoprotein metabolism and ketogenic diets. Dr. Jeff Volek is a Professor in the Department of Human Sciences at The Ohio State University. A world-renowned expert in low carbohydrate research, Dr. Volek focuses on the clinical application of ketogenic diets, especially the management of insulin resistance and type-2 diabetes, as well as athletic performance and recovery. His research aims to understand individual variability including how ketogenic diets alter fatty acid composition, lipoprotein metabolism, gut microbiome, gene expression, adaptations to training and overall metabolic health. He has performed several prospective diet studies that demonstrate that well-formulated ketogenic diets result in substantial improvements in (if not complete reversal of) metabolic syndrome and type-2 diabetes.

I have included an 9 minute video he has on YouTube that discusses the advantages of a low carb diet, how to set one up and the nutrients ratios necessary

Why is a low carbohydrate good for you

The research Dr. Jeff Volek did in 2014 found that total saturated fat in the blood did not increase with a diet high in saturated fats – and went down in most people – despite being increased in the diet when carbs were reduced. Palmitoleic acid, a fatty acid associated with unhealthy metabolism of carbohydrates that can promote disease, went down with low-carb intake and gradually increased as carbs were re-introduced to the study diet. In the study, participants were fed six three-week diets that progressively increased carbs while simultaneously reducing total fat and saturated fat, keeping calories and protein the same.

Effects of Step-Wise Increases in Dietary Carbohydrate on Circulating Saturated Fatty Acids and Palmitoleic Acid in Adults with Metabolic Syndrome

Recent meta-analyses have found no association between heart disease and dietary saturated fat;
however, higher proportions of plasma saturated fatty acids (SFA) predict greater risk for developing type-2 diabetes and heart disease. These observations suggest a disconnect between dietary saturated fat and plasma SFA, but few controlled feeding studies have specifically examined how varying saturated fat intake across a broad range affects circulating SFA levels. Sixteen adults with metabolic syndrome (age 44.9±9.9 yr, BMI 37.9±6.3 kg/m2) were fed six 3-wk diets that progressively increased carbohydrate (from 47 to 346 g/day) with concomitant decreases in total and saturated fat. Despite a distinct increase in saturated fat intake from baseline to the low-carbohydrate diet (46 to 84 g/day), and then a gradual decrease in saturated fat to 32 g/day at the highest carbohydrate phase, there were no significant changes in the proportion of total SFA in any plasma lipid fractions. Whereas plasma saturated fat remained relatively stable, the proportion of palmitoleic acid in plasma triglyceride and cholesteryl ester was significantly and uniformly reduced as carbohydrate intake decreased, and then gradually increased as dietary carbohydrate was re-introduced. The results show that dietary and plasma saturated fat are not related, and that increasing dietary carbohydrate across a range of intakes promotes incremental increases in plasma palmitoleic acid, a biomarker consistently associated with adverse health outcomes.


A cornerstone of dietary guidelines has been the restriction of saturated fat, but that position is now being questioned in large part because recent analyses have found that saturated fat intake is unrelated to risk of disease [2]. However, a higher proportion of plasma saturated fat is related to increased risk of diabetes and heart disease. Thus, there is a need to better understand the relationship between dietary and plasma saturated fat. In this study, we sought to shed light on the impact of replacing saturated fat with carbohydrate on plasma fatty acid composition. Subjects were studied over 21 wk while consuming diets that were progressively higher in carbohydrate and lower in fat. This ‘dose response’ protocol involved six levels of carbohydrate, which allowed us to examine how a wide range of carbohydrate increments affected plasma fatty acid composition within the same person. The results showed that increasing intake of dietary saturated fat did not accumulate in plasma lipid fractions when carbohydrate was restricted, and moreover when dietary saturated fat intake was decreased there was not a consistent decrease in plasma saturated fat. Whereas plasma saturated fat did not associate with dietary carbohydrate or saturated fat; plasma palmitoleic acid, a biomarker associated with increased risk of hyperglycemia, insulin resistance, metabolic syndrome, and type-2 diabetes, tracked incrementally with dietary carbohydrate.

Several lines of evidence point to endogenously produced palmitoleic acid (i.e., cis-16:1n-7) as being associated with dietary carbohydrate intake. In a large population consuming high-carbohydrate diets, there were incremental increases in erythrocyte palmitoleic acid across quartiles of carbohydrate intake ranging from 273 to 419 g/day [9]. In our previous hypocaloric and isocaloric very low-carbohydrate diet studies, we observed consistent decreases in plasma palmitoleic acid independent of fat composition and weight loss. The current results provide additional data that dietary carbohydrate is a primary driver of plasma palmitoleic acid. Subjects who progressively increased carbohydrate from 47 to 346 g/day showed a step-wise increase in plasma palmitoleic acid.

There was remarkable uniformity in the pattern of plasma palmitoleic acid responses as a function of dietary carbohydrate, although the individual trajectories varied. There was also significant variability between individuals during each diet phase with greater variance as carbohydrate increased (Fig 3B). For example, at a carbohydrate intake of 47 g/day TG palmitoleic acid varied from ∼2 to 4 wt%, whereas at 346 g/day it varied from 2 to 7 wt%. Higher proportions of palmitoleic acid in blood or adipose tissue are consistently associated with a myriad of undesirable outcomes such as obesity [27], [28], hypertriglyceridemia [29], hyperglycemia [15], inflammation [30], [31], metabolic syndrome [8], [9], [30], type-2 diabetes [10][14], coronary disease [32], heart failure [33], and incidence and aggressiveness of prostate cancer [21]. It is difficult to assign a specific threshold above which palmitoleic acid confers an increased risk of developing these conditions. In the Physician's Health Study a one standard deviation increase in plasma palmitoleic acid was associated with a 17% higher odds ratio of congestive heart failure [33]. In obese subjects who lost significant weight, higher adipose tissue palmitoleic acid before the diet was associated with failure to maintain weight loss [27]. Since the presence of palmitoleic acid is an indicator of de novo fatty acid synthesis [3], as there is little palmitoleate in common dietary fats, its rising proportion may serve as a proxy of carbohydrate flux through non-oxidative disposal pathways and a harbinger of adverse clinical outcomes.

In regards to total plasma SFA, the pattern of response was more variable than palmitoleic acid. Similar to our previous studies [24], [25], when dietary saturated fat was increased in the context of a very low-carbohydrate intake, the proportion of total plasma SFA was not increased. In this study saturated fat intake at baseline was increased by 38 g/day at C1 through regular consumption of whole eggs, full fat dairy, and high-fat meats. The lack of accumulation of this additional saturated fat was likely due in part to greater oxidation of SFA, as indicated by the significant decrease in respiratory exchange ratio during C1. Whole body fat oxidation increases markedly when dietary carbohydrate is restricted [34], and it is likely that SFA become preferred substrates for beta-oxidation in low-carbohydrate-adapted individuals.

Carbohydrate-induced insulin secretion stimulates DNL and potently suppresses lipolysis and fat oxidation [35], which would promote accumulation of endogenous SFA even when they are reduced in the diet. In the current study, dietary saturated fat was decreased by more than half from C1 to C6 (84 to 32 g/day), yet the majority of participants showed a numerical increase in plasma SFA in all lipid fractions over this same time period. The relative contribution of DNL and fat oxidation and their sensitivity to dietary carbohydrate manipulation likely varies considerably between people and explains the less uniform response in total plasma SFA observed in the current study. However, the pattern of lower plasma SFA after the low-carbohydrate diet with the highest amount of saturated fat, and numerically higher plasma SFA after the high-carbohydrate diet with the least amount of saturated fat, is consistent with the regulation of DNL and fat oxidation by carbohydrate intake and its effect on the glucose-insulin axis.

The reduced proportion of plasma palmitoleic acid after the low-carbohydrate diet was associated with positive responses in other traditional risk markers. Serum triglycerides, glucose, insulin, and estimates of insulin sensitivity were improved as well. Serum cholesterol responses were variable but consistent with the known effects of carbohydrate restriction to increase, on average, total cholesterol, HDL-C and LDL-C relative to low-fat diets [36].

There were several limitations in this study. The diet phases were relatively short to keep the entire feeding portion of study less than 6 months, and by design we created menus that were hypocaloric to induce weight loss. The highest carbohydrate intake was only 55% of total energy and it was consumed in the context of a daily caloric deficit and ongoing weight loss for most subject. Whether carbohydrate-induced increases in plasma palmitoleic acid would have been similar or more pronounced in the context of eucaloric weight maintenance diets remains unknown. Furthermore, since subjects initially restricted carbohydrates and then sequentially added them back over time it is difficult to disassociate temporal changes that may be influenced by cumulative weight loss or lingering effects from the previous diet phases. To address this limitation we provided the diets in reverse order (i.e., high- to low-carbohydrate) to a small number of participants (n = 5). In these individuals, plasma palmitoleic acid responded in the exact opposite pattern as the primary group providing strong evidence that the major driver of circulating palmitoleic acid was the level of carbohydrate in the diet, and was not significantly modified by the order of diets, length of each diet phase, or weight loss (data not shown).

In summary, high intakes of saturated fat (including regular consumption of whole eggs, full-fat dairy, high-fat beef and other meats) does not contribute to accumulation of plasma SFA in the context of a low carbohydrate intake. A progressive decrease in saturated fat and commensurate increase in carbohydrate intake, on the other hand, is associated with incremental increases in the proportion of plasma palmitoleic acid, which may be signaling impaired metabolism of carbohydrate, even under conditions of negative energy balance and significant weight loss. These findings contradict the perspective that dietary saturated fat per se is harmful, and underscore the importance of considering the level of dietary carbohydrate that accompanies saturated fat consumption.
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