calorie restriction diet (CRD) primate study results
 

Knowing almost nil on the subject, I recently wondered whether my 40+lb accidental weight loss (due to PD) might possibly be my body's attempt to protect my dopamine-producing cells.

Like many of us, swallowing difficulties, loss of sense of smell or taste, fatigue and other PD symptoms, I am on a de facto (as opposed to intentional) CRD. The newly released results of this 20-year primate study speak to the longevity benefit of CRD.

If CRD slows down aging, does it stand to reason that it might slow down PD disease progression? Who here can enlighten me?

http://sciencenow.sciencemag.org/cgi...ull/2009/709/1

Calorie-Counting Monkeys Live Longer

From Science:

Monkeys Rodents, yeast, and roundworms all have something in common: They live longer when they consume less. Now a primate has joined the calorie-restriction club. After 20 long years of waiting, scientists have concluded that rhesus monkeys that eat nearly a third less food than normal monkeys age more slowly. The results come as close as any can to proving that calorie restriction could significantly slow aging in humans--even if such a lean diet would not appeal to most of us. Researchers first discovered the connection between lean diets and extended life spans in a 1935 study of calorie-restricted rats. In the past decade, studies in yeast and worms have pinpointed some genes that may be responsible. Scientists believe the genes somehow ramp up systems to protect an organism from environmental stress and may have evolved to help organisms survive in environments where food was scarce. In rodent studies, calorie restriction can extend life span by 20% to 80%. Whether calorie restriction also slows aging in primates wasn't known, however.

Rose,

This is a really interesting hypothesis, and it makes me think of something I was just reading at the PD Online Research site (sorry, I'm not yet allowed to add links). One area for further study discussed the role of compensatory mechanisms in PD. Apparently, our body does compensate in some ways for the disease prior to becoming symptomatic. In my case, I inexplicably lost around 10 lbs. around 3-4 years before becoming symptomatic- my weight has actually gone up since diagnosis. I think this might be a promising area of research especially, if as suggested at the PD site, it is also done with attention paid to biomarkers, so we might "catch" the disease before we lose 70-80% of our dopamine levels.
While we might consider the weight loss post diagnosis a compensatory measure, some might explain it away as going hand in hand with losing sense of smell and/or taste- results in decreased appetite. Also,
what role do meds play in this? A side effect of some agonists is decreased appetite and weight loss.

Any other thoughts?

1: J Neurochem. 2003 Feb;84(3):417-31.

Meal size and frequency affect neuronal plasticity and vulnerability to disease:
cellular and molecular mechanisms.

Mattson MP, Duan W, Guo Z.

Laboratory of Neurosciences, National Institute on Aging, Gerontology Research
Center, Baltimore, Maryland 21224, USA.

Although all cells in the body require energy to survive and function properly,
excessive calorie intake over long time periods can compromise cell function and
promote disorders such as cardiovascular disease, type-2 diabetes and cancers.
Accordingly, dietary restriction (DR; either caloric restriction or intermittent
fasting, with maintained vitamin and mineral intake) can extend lifespan and can
increase disease resistance. Recent studies have shown that DR can have profound
effects on brain function and vulnerability to injury and disease. DR can
protect neurons against degeneration in animal models of Alzheimer's,
Parkinson's and Huntington's diseases and stroke. Moreover, DR can stimulate the
production of new neurons from stem cells (neurogenesis) and can enhance
synaptic plasticity, which may increase the ability of the brain to resist aging
and restore function following injury. Interestingly, increasing the time
interval between meals can have beneficial effects on the brain and overall
health of mice that are independent of cumulative calorie intake. The beneficial
effects of DR, particularly those of intermittent fasting, appear to be the
result of a cellular stress response that stimulates the production of proteins
that enhance neuronal plasticity and resistance to oxidative and metabolic
insults; they include neurotrophic factors such as brain-derived neurotrophic
factor (BDNF), protein chaperones such as heat-shock proteins, and mitochondrial
uncoupling proteins. Some beneficial effects of DR can be achieved by
administering hormones that suppress appetite (leptin and ciliary neurotrophic
factor) or by supplementing the diet with 2-deoxy-d-glucose, which may act as a
calorie restriction mimetic. The profound influences of the quantity and timing
of food intake on neuronal function and vulnerability to disease have revealed
novel molecular and cellular mechanisms whereby diet affects the nervous system,
and are leading to novel preventative and therapeutic approaches for
neurodegenerative disorders.

PMID: 12558961 [PubMed - indexed for MEDLINE]