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Health news:
June 2010 - Dec 2013

Minimizing breast cancer risk

May 2010

Time to move beyond salt ?

Salt hypothesis vs. reality

Is sodium bad?

April 2010

Salt studies: the latest score

From Dahl to INTERSALT

Salt hypothesis' story

March 2010

Salt war

Do bone drugs work?

Diabetes vs. drugs, 3:0?

February 2010

The MMR vaccine war: Wakefield vs. ?

Wakefield proceedings: an exception?

Who's afraid of a littl' 1998 study?

January 2010

Antibiotic children

Physical activity benefits late-life health

Healthier life for New Year's resolution


December 2009

Autism epidemic worsening: CDC report

Rosuvastatin indication broadened

High-protein diet effects


November 2009

Folic acid cancer risk

Folic acid studies: message in a bottle?

Sweet, short life on a sugary diet


October 2009

Smoking health hazards: no dose-response

C. difficile warning

Asthma risk and waist size in women


September 2009

Antioxidants' melanoma risk: 4-fold or none?

Murky waters of vitamin D status

Is vitamin D deficiency hurting you?


August 2009

Pill-crushing children

New gut test for children and adults

Unhealthy habits - whistling past the graveyard?


July 2009

Asthma solution - between two opposites that don't attract

Light wave therapy - how does it actually work?

Hodgkin's lymphoma in children: better alternatives


June 2009

Hodgkin's, kids, and the abuse of power

Efficacy and safety of the conventional treatment for Hodgkin's:
behind the hype

Long-term mortality and morbidity after conventional treatments for pediatric Hodgkin's


May 2009

Late health effects of the toxicity of the conventional treatment for Hodgkin's

Daniel's true 5-year chances with the conventional treatment for Hodgkin's

Daniel Hauser Hodgkin's case: child protection or medical oppression?

April 2009

Protection from EMF: you're on your own

EMF pollution battle: same old...

EMF health threat and the politics of status quo

March 2009

Electromagnetic danger? No such thing, in our view...

EMF safety standards: are they safe?

Power-frequency field exposure

February 2009

Electricity and health

Electromagnetic spectrum: health connection

Is power pollution making you sick?

January 2009

Pneumococcal vaccine for adults useless?

DHA in brain development study - why not boys?

HRT shrinks brains


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May 2008

Obesity and the brain

Obesity's bad reputation of causing or aggravating diseases has recently been expanded to include significantly higher risk for developing dementia and even Alzheimer's. Obesity and brain? Yes, you read it right. And it seems to be making a lot of sense.

According to the results of recently published study (Whitmer et al, Neurology journal, March 2008) on over 6500 individuals within 36-year time span, those that were obese, with large belly, were

3.6 times more likely to develop dementia

than those with normal body weight and belly size (obesity without large belly increased the risk 2.7 times).

One of the reasons why it shouldn't be surprising - except, perhaps, for the magnitude - is that obese folks are much more likely to have elevated glucose level or full-blown diabetes. While the specifics of how exactly the elevated glucose level damages memory are yet to be explained, recent evidence of it being a significant factor in developing dementia and Alzheimer's is conclusive. Neural cells, in general, are

more sensitive to the restriction in production of cellular energy

due to inefficient insulin function (with glucose, as a result, accumulating in the blood instead of being transferred into the cells and burned for energy). Impaired memory being one of its longer-term consequences only seems logical.

Another reason has to do with obesity being restricting mobility. It is known for some time now that regular physical activity stimulates production of new neural cells in the portion of hippocampus - curved ridge of neural tissue in the middle of each brain hemisphere - where the memory is processed. Both, dementia and Alzheimer's sufferers have

 significantly reduced hippocampus volume,

although the node that is affected is not identical for the two. The one affected in dementia is where neural cells production continues throughout the lifetime. Reduced physical activity would result in slower growth of this node, its smaller size and, possibly, lower functional capacity.

Are these two factors - elevated blood glucose and reduced mobility, typical for obese individuals - really causing dementia, or only contributing to it? Elevated blood glucose, indicating its compromised cellular supply and energy production, if severe enough, could contribute to accelerated rate of dying and longer-term impairment in the memory function resulting from it.

Also, lower energy level can certainly make the cells more vulnerable to both, chemical toxins and effects of nutritional deficiencies. The consequence can be the onset of dementia, as well as Alzheimer's, as this recent research suggests.

As for the reduced production of neural cells in the hippocampus due to low physical activity, it alone is probably not likely to result in dementia. But if your cells begin to die at an accelerated rate due to any of a number of possible factors, the fewer total of cells you have in this part of brain, the sooner you'll feel the consequences.

In all, seems that we can add one more legitimate reason - keeping brain function from accelerated onset of dementia - to already quite extensive list of reasons why not to take on too many extra pounds. þ