High MUFA Diets are (Heart-)Healthy and Probably Superior to High PUFA Diets

Ever since the "Mediterranean Diet" was/is the talk of the town, more and more people become aware of the potential benefits of the formerly largely ignored mono-unsaturated fatty acids (MUFAs). In spite of that, the majority of consumers (probably due to the misinformation coming from the marketing machinery of the food industry) still focuses on avoiding the "bad" saturated fats and consuming as much "healthy" polyunsaturated fats (PUFAs) as possible in order not to fall victim to an obesity epidemic which is inseparably intertwined with these kind of black-and-white approaches to nutrition.

In an extensive review (Jones. 2011) scientists from the Department of Human Nutritional Sciences at the Richardson Centre for Functional Foods and Nutraceuticals (University of Manitoba, Canada) evaluated data from over 50 years of research to come to the conclusion:

Consumption of dietary MUFA promotes healthy blood lipid profiles, mediates blood pressure, improves insulin sensitivity and regulates glucose levels. Moreover, provocative newer data suggest a role for preferential oxidation and metabolism of dietary MUFA, influencing body composition and ameliorating the risk of obesity. Mounting epidemiological and human clinical trial data continue to demonstrate the cardioprotective activity of the MUFA content of dietary fat.

In fact, they found MUFA rich diets to be superior even to diets enriched in PUFAs, which have lately oftentimes been hailed as the saviors of the fat and unhealthy:

When PUFA and MUFA rich diets were compared for replacement of dietary SFA in healthy adult subjects, those consuming MUFA rich diets demonstrated a preservation of HDL-C levels to a greater extent with only a 4% decrease in HDL-C levels compared to those consuming PUFA rich diets, which decreased HDL-C levels by 14%.

What is interesting, however, is that there still seems to be an initial bias against saturated fatty acids. This can also be seen from the fact that the general questions the authors pose throughout their review always come back to the idea of replacing saturated fatty acids by either carbs or MUFA, PUFA or MUFA etc. I would be interested to see a study or a review without this initial bias against saturated fats - the results could be very interesting... what do you think?

Scientific Evidence Links High Carbohydrate Intake to the Development of Alzheimer's and Other Neurological Diseases

"Fats are bad, carbs are healthy!" I hope nobody out there still believes this late 20th Century slogan. If you do, chances are you will soon forget about it due to the neuronal damage you are inflicting to your brain by eating a high carb diet.

In a very recent review, a group of international scientists (Seneff. 2011) summarize the current state of research as follows:

[...] an excess of dietary carbohydrates, particularly fructose, alongside a relative deficiency in dietary fats and cholesterol, may lead to the development of Alzheimer's disease. A first step in the pathophysiology of the disease is represented by advanced glycation end-products in crucial plasma proteins concerned with fat, cholesterol, and oxygen transport. This leads to cholesterol deficiency in neurons, which significantly impairs their ability to function. Over time, a cascade response leads to impaired glutamate signaling, increased oxidative damage, mitochondrial and lysosomal dysfunction, increased risk to microbial infection, and, ultimately, apoptosis. 

They also compiled a comprehensive list of take-home-massages, some of which may have far reaching consequences:

• Researchers have identified mitochondrial dysfunction and brain insulin resistance as early indicators of Alzheimer's disease.

• ApoE-4 is a risk factor for Alzheimer's disease, and ApoE is involved in the transport of cholesterol and fats, which are essential for signal transduction and protection from oxidative damage.

• The cerebrospinal fluid of Alzheimer's brains is deficient in fats and cholesterol.

• Advanced glycation end-products (AGEs) are present in significant amounts in Alzheimer's brains.

• Fructose, an increasingly pervasive sweetening agent, is ten times as reactive as glucose in inducing AGEs.

• Astrocytes play an important role in providing fat and cholesterol to neurons. [...]

• Glycation damage interferes with the LDL-mediated delivery of fats and cholesterol to astrocytes, and therefore, indirectly, to neurons. [...]

• Synthesis of the neurotransmitter, glutamate, is increased when cholesterol is deficient, and glutamate is a potent oxidizing agent.

• Over time, neurons become severely damaged due to chronic exposure to glucose and oxidizing agents, and are programmed for apoptosis due to highly impaired function. [...]

• Simple dietary modification, towards fewer highly-processed carbohydrates and relatively more fats and cholesterol, is likely a protective measure against Alzheimer's disease.

So, if you have not already forgotten what you just read, make sure to cut back your carbohydrate consumption, limit fructose intake and stop being afraid of fats and cholesterol before you cannot remember anymore.

Pot Belly and High Triglycerides Indicative of Low LDL & HDL Particle Size

A recent study by scientists from the Mayo Clinic in Minnesota (Irving. 2011) found that the most reliable indicators of LDL & HDL particle size in 84 healthy non-diabetic men and women were a huge amount of trunk fat and high triglyceride levels.

[...] the accumulation of atherogenic lipoprotein particles (e.g. small, dense, low-density lipoprotein particles and small, high-density lipoprotein particles) was associated with low levels of insulin sensitivity, cardiorespiratory fitness, and higher levels of adiposity. However, multivariate forward-stepwise regression revealed that triglycerides, followed by truncal fat mass, were the strongest predictors of the lipoprotein particle size and concentration data.

These results are of particular interest to those who cannot afford having a comprehensive lipid panel done. Since the standard tests often do not provide any information about the size of the cholesterol particles, looking and triglycerides and truncal fat may be a useful indicator of whether or not it will be necessary to check cholesterol particle sizes, as well.

On a side note: Other than it has long been thought, current research suggests that neither the amount of total cholesterol, nor the amount of LDL cholesterol, but rather the size of the cholesterol lipo-proteins is the main determinant of how likely one is to develop arteriosclerosis: Large particle size = benign; small particle size = dangerous.

1.200 IU Vitamin D Won't Raise 25OH-D Levels Enough to See Beneficial Effects on Markers of Cardiovascular Health

In the course of the last weeks, I have refrained from posting each of the 1001 studies on vitamin D that appear in the myriad of medical magazines each month. It is simply too much, mostly very irrelevant information. A recent study by Maki et al. (Maki. 2011) is yet interesting insofar, as it provides some insight into the amounts of supplemental vitamin D one would probably need to see some cardiovascular benefits.

After supplementing the diets of their subjects with either a standard multi-vitamin or the multi-vitamin + 1,200IU of vitamin D for 8 weeks, the researcers measured serum 25-hydroxyvitamin D [25(OH)D] and high-density lipoprotein cholesterol (HDL-C) in subjects with high waist circumference and found:

There was a significant difference in mean change for 25(OH)D between the MVM and MVM+D treatment groups ( − 1.2 ± 2.5 nmol/l vs. 11.7 ± 3.0 nmol/l, respectively; P = 0.003). Vitamin D 1,200 IU/day did not increase 25(OH)D to a desirable level ( ≥ 75 nmol/l) in 61% of participants. There were no significant changes in cardiovascular disease risk markers. 

This is quite interesting, because even after all the fuss about vitamin D defiency that has even reached the mass media in the course of the last months, the general recommendation is not to take more than 1.000IU of vitamin D (sometimes even less) per day. For most people, this study seems to indicate, this is far too little to even get their vitamin D levels into the desirable ranges. Whether or not this would provide them with the beneficial results many scientists hope for, remains to be elucidated, though.

Even Individuals on a "Healthy" Diet May Benefit from Supplemental Fiber

Fiber has been advertised for years as a universal health promoter. It curves appetite, reduces cholesterol and improves digestion - but is it really necessary to supplement with additional fiber, if your intake in fibrous veggies etc. is already high? A recent study by scientists from Australia (Pal. 2010) suggests that it may not be necessary, yet beneficial.

Figure 1: Changes in body weight (A); BMI (B); % body fat (C) and waist circumference (D).
From left to right: Control, FIB, HLT, HLT-FIB

Studying a cohort of 72 overweight and obese individuals with a BMI between 25 and 40 kg/m² and age between 18 and 65 years, the researchers found that over a time period of 12 weeks in which the subjects either practiced their "normal" eating habits or changed to a healthy food diet (HFT), supplemented with fiber (FIB) or switched to a healthy food diet that was supplemented with fiber (HFT-FIB)...

[...] weight, BMI and % total body fat were significantly reduced in FIB and HLT–FIB groups, with weight and BMI significantly reduced in the HLT group compared with control at 12 weeks. HLT–FIB and HLT groups had significant reductions in TAG and insulin compared with control at 6 and 12 weeks, and in insulin compared with the FIB group at 12 weeks. The HLT–FIB, HLT and FIB groups all had significant reductions in total cholesterol and LDL-cholesterol compared with control after 6 and 12 weeks.

As can be seen from figure 1 (above) the addition of fiber to an already healthy diet did in fact improve the overall beneficial results of the change in dietary habits. Bottom line: Firstly, eat healthy! Secondly, consider using a fiber supplement only if your diet is already in check.