Anti-CRON, less ALS?

[Guest guest]

Hi All,

The below paper on the surface appears to implicate a high calorie diet with the

disease from which Roy Walford died. The pdf of the paper is available.

Reasonably, being alive, but suffering brain cell death, may be not preferred.

My

impression is that ketones appear to protect from such

http://en.wikipedia.org/wiki/Amyotrophic_lateral_sclerosis (ALS) pathologies, as

also suggested for seizures. It may be that the % caloric composition, fat 60%,

carbohydrate 20%, protein 20%, diet may lead to greater death from causes in

addition to the greatly increased deaths due to ALS or seizures. If we are not

at

risk of seizures nor ALS, we may die earlier on the caloric composition, fat

60%,

carbohydrate 20%, protein 20% diet (see the concluding excerpt from the

full-text).

We may also suffer more illnesses. First, is an introduction.

Source: The Mount Sinai Hospital / Mount Sinai School of Medicine

Posted: April 18, 2006

High Caloric Diet May Prevent Progression Of Amyotrophic Lateral Sclerosis

(ALS)

A recent study directed by the Mount Sinai School of Medicine suggests a

ketogenic- high caloric diet may prevent the progression of Amyotrophic Lateral

Sclerosis (ALS). This study, which appears in the April 3, 2006 issue of BMC

Neuroscience

... " The findings assert the significance of certain high caloric dietary

intake in the prevention of ALS. In view of any available therapeutic

application

for the disease, this new evidence might bring hope to those affected. "

Zhao Z, Lange DJ, Voustianiouk A, MacGrogan D, Ho L, Suh J, Humala N,

Thiyagarajan

M, Wang J, Pasinetti GM.

A ketogenic diet as a potential novel therapeutic intervention in amyotrophic

lateral sclerosis.

BMC Neurosci. 2006 Apr 3;7:29.

PMID: 16584562 http://tinyurl.com/qs88f

... SOD1-G93A transgenic ALS mice were fed a ketogenic diet (KD) based on

known

formulations for humans. Motor performance, longevity, and motor neuron counts

were

measured in treated and disease controls. Because mitochondrial dysfunction

plays a

central role in neuronal cell death in ALS, we also studied the effect that the

principal ketone body, D-beta-3 hydroxybutyrate (DBH), has on mitochondrial ATP

generation and neuroprotection. Blood ketones were > 3.5 times higher in KD fed

animals compared to controls. KD fed mice lost 50% of baseline motor performance

25

days later than disease controls. KD animals weighed 4.6 g more than disease

control

animals at study endpoint; the interaction between diet and change in weight was

significant (p = 0.047). In spinal cord sections obtained at the study endpoint,

there were more motor neurons in KD fed animals (p = 0.030). DBH prevented

rotenone

mediated inhibition of mitochondrial complex I but not malonate inhibition of

complex II. Rotenone neurotoxicity in SMI-32 immunopositive motor neurons was

also

inhibited by DBH. CONCLUSION: This is the first study showing that diet,

specifically a KD, alters the progression of the clinical and biological

manifestations of the G93A SOD1 transgenic mouse model of ALS. These effects may

be

due to the ability of ketone bodies to promote ATP synthesis and bypass

inhibition

of complex I in the mitochondrial respiratory chain.

... At 50 days of age animals placed on either a ketogenic diet (caloric

composition, fat 60%, carbohydrate 20%, protein 20%) or a standard rodent

laboratory

diet (fat 10%, carbohydrate 70%, protein 20%). Both diets contained equal

percentages of cholesterol per gram ...

... There was no statistically significant difference in the age at death

between KD fed animals compared to SOD1-G93 transgenic mice fed a standard

laboratory diet (133 ± 4 vs. 131 ± 4 days, p = 0.914) ...

-- Al Pater, alpater@...

__________________________________________________