Beauty Health for Life

University of Granada researchers from the Faculty of Medicine and the Faculty of Physical Activity and Sports Sciences have scientifically disproven the old belief that eating chocolate is fattening. In an article published this week in the journal Nutrition, the authors have shown that higher consumption of chocolate is associated with lower levels of total fat (fat deposited all over the body) and central fat (abdominal), independently of whether or not the individual participates in regular physical activity and of diet, among other factors.

The researchers determined whether greater chocolate consumption associated with higher body mass index and other indicators of total and central body fat in adolescents participating in the HELENA (Healthy Lifestyle in Europe by Nutrition in Adolescence) study. This project, financed by the European Union, studies eating habits and lifestyle in young people in 9 European countries, including Spain.


Independent of diet and physical activity

The study involved 1458 adolescents aged between 12 and 17 years and results showed that a higher level of chocolate consumption associated with lower levels of total and central fat when these were estimated through body mass index, body fat percentage—measured by both skinfolds and bioelectrical impedance analysis—and waist circumference. These results were independent of the participants sex, age, sexual maturation, total energy intake, intake of saturated fats, fruit and vegetables, consumption of tea and coffee, and physical activity.

As the principle author Magdalena Cuenca-García explains, although chocolate is considered a high energy content food—it is rich in sugars and saturated fats—“recent studies in adults suggest chocolate consumption is associated with a lower risk of cardiometabolic disorders”.

In fact, chocolate is rich in flavonoids—especially catechins—which have many healthy properties: “they have important antioxidant, antithrombotic, anti-inflammatory and antihypertensive effects and can help prevent ischemic heart disease”.

Recently, another cross-sectional study in adults conducted by University of California researchers found that more frequent chocolate consumption also associated with a lower body mass index. Whats more, these results were confirmed in a longitudinal study in women who followed a catechin-rich diet.

The effect could be partly due to the influence of catechins on cortisol production and on insulin sensitivity, both of which are related with overweight and obesity.


Calorie impact is not the only thing that matters

The University of Granada researchers have sought to go further and analyse the effect of chocolate consumption at a critical age like adolescence by also controlling other factors that could influence the accumulation of fat. The research, which is both novel and, perhaps, the largest and best-controlled study to date, is the first to focus on the adolescent population. It includes a large number of body measures, objective measurement of physical activity, detailed dietary recall with 2 non-consecutive 24-hour registers using image-based software, and controls for the possible effect of a group of key variables.

In Nutrition, the authors stress that the biological impact of foods should not be evaluated solely in terms of calories. “The most recent epidemiologic research focuses on studying the relation between specific foods—both for their calorie content and for their components—and the risk factors for developing chronic illnesses, including overweight and obesity”.

Despite their results, the authors insist that chocolate consumption should always be moderate. “In moderate quantities, chocolate can be good for you, as our study has shown. But, undoubtedly, excessive consumption is prejudicial. As they say: you can have too much of a good thing”.

The University of Granada researchers stress that their findings “are also important from a clinical perspective since they contribute to our understanding of the factors underlying the control and maintenance of optimal weight”.

Although problems with memory become increasingly common as people age, in some persons, memories last long time, even a life time. On the other hand, some people experience milder to substantial memory problems even at an earlier age.

Although there are several risk factors of dementia, abnormal fat metabolism has been known to pose a risk for memory and learning. People with high amounts of abdominal fat in their middle age are 3.6 times as likely to develop memory loss and dementia later in their life.

Neurological scientists at the Rush University Medical Center in collaboration with the National Institutes of Health have discovered that same protein that controls fat metabolism in the liver resides in the memory center of the brain (hippocampus) and controls memory and learning.

Results from the study funded by the Alzheimer’s Association and the National Institutes of Health were recently published in Cell Reports.

“We need to better understand how fat is connected to memory and learning so that we can develop effective approach to protect memory and learning,” said Kalipada Pahan, PhD, the Floyd A. Davis professor of neurology at Rush University Medical Center.

The liver is the body’s major fat metabolizing organ. Peroxisome proliferator-activated receptor alpha (PPARalpha) is known to control fat metabolism in the liver. Accordingly, PPARalpha is highly expressed in the liver.

“We are surprised to find high level of PPARalpha in the hippocampus of animal models,” said Pahan.

“While PPARalpha deficient mice are poor in learning and memory, injection of PPARα to the hippocampus of PPARalpha deficient mice improves learning and memory," said Pahan.

Since PPARalpha directly controls fat metabolism, people with abdominal fat levels have depleted PPARalpha in the liver and abnormal lipid metabolism. At first, these individuals lose PPARalpha from the liver and then eventually from the whole body including the brain. Theore, abdominal fat is an early indication of some kind of dementia later in life, according to Pahan.

By bone marrow chimera technique, researchers were able to create some mice having normal PPARalpha in the liver and depleted PPARalpha in the brain. These mice were poor in memory and learning. On the other hand, mice that have normal PPARalpha in the brain and depleted PPARalpha in the liver showed normal memory.

“Our study indicates that people may suffer from memory-related problems only when they lose PPARalpha in the hippocampus”, said Pahan.

CREB (cyclic AMP response element-binding protein) is called the master regulator of memory as it controls different memory-related proteins. “Our study shows that PPARalpha directly stimulates CREB and thereby increases memory-related proteins”, said Pahan.

“Further research must be conducted to see how we could potentially maintain normal PPARalpha in the brain in order to be resistant to memory loss”, said Pahan.

Other Rush researchers involved in this study include Avik Roy, PhD, research assistant professor; Malabendu Jana, PhD assistant professor; Grant Corbett, neuroscience graduate student; Shilpa Ramaswamy, instructor; and Jeffrey H. Kordower, PhD, the Jean Schweppe Armour professor of neurological sciences.

Alzheimer’s disease is the most common human disorder associated with memory loss. This disease slowly destroys memory and thinking skills, and eventually even the ability to carry out the simplest tasks. Nationwide, the total payments for services for people with Alzheimer’s and other forms of dementia will total $203 billion in 2013. By 2050, the total costs are expected to increase 500 percent to a staggering $1.2 trillion.

It isnt just carbohydrates people with diabetes need to be vigilant about. Its the fat too.

A new study from the Joslin Clinic in Boston found that patients with type 1 diabetes required more insulin coverage for a higher-fat meal compared to a lower-fat meal. The meals were prepared in the Clinics kitchen and had identical carbohydrate and protein, but different fat content - 60 grams vs. 10 grams. The carbohydrates in the meals had similar glycemic indexes.

Dietary Fat Acutely Increases Glucose Concentrations and Insulin Requirements in Patients With Type 1 Diabetes, Diabetes Care, April 2013

It was a small study of crossover design, meaning each participant consumed both the high-fat meal and the low-fat meal.

"RESULTS Seven patients with type 1 diabetes (age, 55 ± 12 years; A1C 7.2 ± 0.8%) successfully completed the protocol. [The high-fat] dinner required more insulin than [the low-fat] dinner (12.6 ± 1.9 units vs. 9.0 ± 1.3 units; P = 0.01) and, despite the additional insulin, caused more hyperglycemia.

CONCLUSIONS This evidence that dietary fat increases glucose levels and insulin requirements highlights the limitations of the current carbohydrate-based approach to bolus dose calculation. These findings point to the need for alternative insulin dosing algorithms for higher-fat meals and suggest that dietary fat intake is an important nutritional consideration for glycemic control in individuals with type 1 diabetes."

Joslin accompanied their study with this short video:

"When people ate a higher fat meal, their blood sugars were higher for longer and required more insulin."

Why does dietary fat lead to higher blood glucose? It is thought that fat contributes to insulin resistance:

"Dietary fat and free fatty acids (FFAs) are known to impair insulin sensitivity and to enhance hepatic glucose production. ... Interventions that lower [free fatty acid] levels in nondiabetic and type 2 diabetic individuals lead to both improved insulin sensitivity and glucose tolerance."

Saturated fat may be more problematic:

"Studies in nondiabetic individuals indicate that saturated fats cause more profound insulin resistance than monounsaturated and polyunsaturated fats. By design, the [high-fat] dinner meal in the current study was predominantly saturated fat."

And:

"Pizza is widely recognized to cause marked late postprandial hyperglycemia in patients with type 1 diabetes."

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