Ketogenic Diet - Powerful Dietary Strategy for Certain Conditions

Laura

Administrator
Administrator
Moderator
FOTCM Member
Re: Ketogenic Diet - Path To Transformation?

Megan, start with this one (PDF):
http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&ved=0CGwQFjAB&url=http%3A%2F%2Fsurvivalbiology.files.wordpress.com%2F2011%2F08%2Fmitochondrial-energetics-douglas-c-wallace.pdf&ei=8OEeULrxDajV0QXmgIEI&usg=AFQjCNGIBk0aI7QDy7DzjB2AOKs21dB2bw&sig2=I4nR9Tr1_6IhR5mk2jDruA
 
Re: Ketogenic Diet - Path To Transformation?

These new findings are allowing me to understand a few reasons as to why I have not developed any significant health issues throughout my life, osit. The skipping of meals on a daily basis along with the periodic true "fasting", if the recent information posted is correct, allowed the body to enter survival mode, cleansing out a lot of the garbage in the body, and using what it did have more efficiently. It explains, in my case, why I never gained a lot of weight, even when I was eating a higher proportion of carbs than fat.

One of the other things that dawned on me was the fact that our paleo ancestors did not eat by a clock the way modern society does. This to me would mean that upon waking at sunrise each morning, once the need to eat arose, it may have taken them hours to hunt down a meal, which being conservative, would put their main meal around what we consider "brunch", or between breakfast and lunch. Due to them being in ketosis, and without modern knowledge of food preservation, they would eat primarily right after the acquisition of the hunt, then maybe a bit of what was leftover- if any- a little later. Due to the ketogenic state, if it were say 16-20 hours between meals, the body would have been in starvation mode, which put cell repair and energy efficiency as the mode of operation.

Obviously this is only my opinion after reading the new information, but it seems the most logical to me. I also wonder if the body being in this mode on a regular basis not only prevented diseases as we know them today, but could be a contributing factor to the much higher bone density of our paleo ancestors than what modern humans have. Definitely looking forward to the more technical papers to be released soon, as hopefully they will shed more light on this subject.

Thanks Laura & team!
 

mb

The Living Force
FOTCM Member
Re: Ketogenic Diet - Path To Transformation?

Laura said:
Megan, start with this one (PDF):
http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&ved=0CGwQFjAB&url=http%3A%2F%2Fsurvivalbiology.files.wordpress.com%2F2011%2F08%2Fmitochondrial-energetics-douglas-c-wallace.pdf&ei=8OEeULrxDajV0QXmgIEI&usg=AFQjCNGIBk0aI7QDy7DzjB2AOKs21dB2bw&sig2=I4nR9Tr1_6IhR5mk2jDruA
I am reading... Wow.

An aside -- it would appear that our metabolic machinery is not designed to operate in high EMF environments. I will have to return to that aspect later (and in a different topic).
 

LQB

The Living Force
FOTCM Member
Re: Ketogenic Diet - Path To Transformation?

Megan said:
Laura said:
Megan, start with this one (PDF):
http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&ved=0CGwQFjAB&url=http%3A%2F%2Fsurvivalbiology.files.wordpress.com%2F2011%2F08%2Fmitochondrial-energetics-douglas-c-wallace.pdf&ei=8OEeULrxDajV0QXmgIEI&usg=AFQjCNGIBk0aI7QDy7DzjB2AOKs21dB2bw&sig2=I4nR9Tr1_6IhR5mk2jDruA
I am reading... Wow.

An aside -- it would appear that our metabolic machinery is not designed to operate in high EMF environments. I will have to return to that aspect later (and in a different topic).
Interesting. The thesis I'm developing on EMF effects ties sensitivity to diet and toxins as well. It seems to be the combined effects that really does folks in.
 

sebbe

Jedi
Re: Ketogenic Diet - Path To Transformation?

Laura :

What struck me as I was reading all this material is this: what if the "ascension process" much touted in esoterica is exactly this: figuring out how to heal and activate DNA? What if, by these studies and experiments, we manage to activate/accelerate "soul seating" capacity and "receivership capability"??? What if this is part of "it's not where you are, but who you are and what you see"? Perhaps, by aligning with our paleolithic ancestors who painted caves and decorated the earth with megaliths, and restoring our DNA to that more similar to theirs, we might acquire, along the way, some of their abilities?
It is very intersting. If i understand correctly, it could be like a reverse ingeneering. From the body to the soul.

I was reading a book. I forget reference, but it was talking about EMDR (EMT). The author explained how carriage of the body could reveal "carriage" of the soul, and how, if we change volontarly these positions of the body, it could affect mind in a more positive way, for recovery. It is perhaps a little similar?
 

SeekinTruth

Ambassador
Ambassador
FOTCM Member
Re: Ketogenic Diet - Path To Transformation?

sebbe said:
Laura :

What struck me as I was reading all this material is this: what if the "ascension process" much touted in esoterica is exactly this: figuring out how to heal and activate DNA? What if, by these studies and experiments, we manage to activate/accelerate "soul seating" capacity and "receivership capability"??? What if this is part of "it's not where you are, but who you are and what you see"? Perhaps, by aligning with our paleolithic ancestors who painted caves and decorated the earth with megaliths, and restoring our DNA to that more similar to theirs, we might acquire, along the way, some of their abilities?
It is very intersting. If i understand correctly, it could be like a reverse ingeneering. From the body to the soul.

I was reading a book. I forget reference, but it was talking about EMDR (EMT). The author explained how carriage of the body could reveal "carriage" of the soul, and how, if we change volontarly these positions of the body, it could affect mind in a more positive way, for recovery. It is perhaps a little similar?
Yeah, that speculation really IS very interesting. I think there's quite a bit of clues/hints and evidence that this may be plausible. In any case I think that any positive epigenetic / gene expression changes will have many beneficial chain reactions down the road, in addition to any other DNA activation that leads to "more receivership capability."

I'm doing a type of intermittent fasting for quite a while by eating just 2 meals a day -- breakfast and dinner. The hours I eat breakfast vary wildly -- anywhere from 9AM to 11:30AM. And dinner swings between 5PM and 6:30PM. I think I'm going try eating a smaller breakfast every other day, or every few days, and either a very small dinner or none, just as an experiment to see what effects it might have on me.
 

Laura

Administrator
Administrator
Moderator
FOTCM Member
Re: Ketogenic Diet - Path To Transformation?

Megan said:
Laura said:
Megan, start with this one (PDF):
http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&ved=0CGwQFjAB&url=http%3A%2F%2Fsurvivalbiology.files.wordpress.com%2F2011%2F08%2Fmitochondrial-energetics-douglas-c-wallace.pdf&ei=8OEeULrxDajV0QXmgIEI&usg=AFQjCNGIBk0aI7QDy7DzjB2AOKs21dB2bw&sig2=I4nR9Tr1_6IhR5mk2jDruA
I am reading... Wow.

An aside -- it would appear that our metabolic machinery is not designed to operate in high EMF environments. I will have to return to that aspect later (and in a different topic).
Having the whole mechanism explained in detail demonstrates that carb fuel downregulates about everything that is very beneficial though it does it in a way that sort of prevents MAJOR damage, until too many carbs are eaten, at which point, the body can no longer cope.

But fueling the body with fats/ketones, UPregulates all the good stuff and can correct the damage done by carb fuel under most circumstances.

One thing that strikes me, putting this material together with the long discussion about DNA mutations in "The 5th Option", is that eating carbs could actually create the conditions for mutations. Not just carbs, of course, but plastic fats and a host of other noxious substances that we take into our bodies.

According to this paper, stuff like lifting weights is better than aerobics because "Resistance exercise activates the proliferation of satellite cells in skeletal muscle as a consequence of muscle fiber injury. The level of mutant mtDNA in satellite cells is generally lower than in mature muscle fibers. Hence, fusion of satellite cells shifts the heteroplasmic level toward the wild-type (non-mutated) mtDNAs, leading to improvement in OXPHOS capacity." (oxidative phosphorylation = how we get energy)
 

aragorn

The Living Force
FOTCM Member
Re: Ketogenic Diet - Path To Transformation?

Laura said:
Megan, start with this one (PDF):
http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&ved=0CGwQFjAB&url=http%3A%2F%2Fsurvivalbiology.files.wordpress.com%2F2011%2F08%2Fmitochondrial-energetics-douglas-c-wallace.pdf&ei=8OEeULrxDajV0QXmgIEI&usg=AFQjCNGIBk0aI7QDy7DzjB2AOKs21dB2bw&sig2=I4nR9Tr1_6IhR5mk2jDruA
Thanks! This was veerrry interesting. I've been VERY frustrated with my low energy levels, even though I'm supposedly "eating right". I've been thinking that there MUST be something missing in the equation - and this fasting thing might just be it. The thing about the different mutant MDNA in different haplogroups was also very interesting.

Yesterday, I wrote to Nora Gedgaudas asking about this low energy/mithocondria thing. I'm not expecting any answer soon, or ever, since she writes that she receives about 100 emails per day. But who knows. ;)
 

Laura

Administrator
Administrator
Moderator
FOTCM Member
Re: Ketogenic Diet - Path To Transformation?

Aragorn said:
Laura said:
Megan, start with this one (PDF):
http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&ved=0CGwQFjAB&url=http%3A%2F%2Fsurvivalbiology.files.wordpress.com%2F2011%2F08%2Fmitochondrial-energetics-douglas-c-wallace.pdf&ei=8OEeULrxDajV0QXmgIEI&usg=AFQjCNGIBk0aI7QDy7DzjB2AOKs21dB2bw&sig2=I4nR9Tr1_6IhR5mk2jDruA
Thanks! This was veerrry interesting. I've been VERY frustrated with my low energy levels, even though I'm supposedly "eating right". I've been thinking that there MUST be something missing in the equation - and this fasting thing might just be it. The thing about the different mutant MDNA in different haplogroups was also very interesting.

Yesterday, I wrote to Nora Gedgaudas asking about this low energy/mithocondria thing. I'm not expecting any answer soon, or ever, since she writes that she receives about 100 emails per day. But who knows. ;)
Yes, the energy problems for the skinny people are apparently different from the energy problems of the plump people, but they are energy problems nonetheless. Seems that what a person needs to do to upregulate mitochondrial biogenesis is ketogenic diet, intermittent fasting, and resistance exercise.
 

nicklebleu

The Living Force
FOTCM Member
Re: Ketogenic Diet - Path To Transformation?

I have been on a low-carb diet for quite a while now, but I also have hit a brick wall - with my weight. I have actually put on some in the last few months ...
Also I had my cholesterol checked (had to for professional reasons), and was a bit shocked:

Cholesterol 10.9 mmol/l (normal 5)
Triglycerides 2.1 mmol/l (normal < 2)
HDL 1.7 mmol/l (normal > 0.7)
LDL 8.2 mmol/l (normal < 3.4)
Ratio 6.4 (average risk 4.9)

I don't attribute much to the cholesterol measurement, but I was a bit surprised that my triglycerides where slightly elevated too.

I have been eating lots of butter in the last few months - and I mean LOTS, like 150g per day. I think I might ease with the butter a bit and also go on to do IF, eat only breakfast on intermittent days.

I just feel that we haven't got to the bottom of all that ... a ketogenic diet surely is a good thing, but seems not to be the end of the story. Seems to me that the issue is a lot more complicated than that. Will do some other test results (TSH and reverse T3 - I am pretty certain I am leptin resistant).
 

Laura

Administrator
Administrator
Moderator
FOTCM Member
Re: Ketogenic Diet - Path To Transformation?

nicklebleu said:
I just feel that we haven't got to the bottom of all that ... a ketogenic diet surely is a good thing, but seems not to be the end of the story. Seems to me that the issue is a lot more complicated than that. Will do some other test results (TSH and reverse T3 - I am pretty certain I am leptin resistant).
You may change your mind about KD after reading all the papers we are going to get the links to posted. I was going in the direction of thinking "oh, some people MUST need more carbs or this or that" because the whole system and what can go wrong and what probably does go wrong was not clear to me. But, when you put KD together with IF and some resistance training rather like what Gedgaudas describes, to stimulate the upregulation of the "wild mtDNA", it all begins to make sense. Obviously, there are going to be people with such damaged mtDNA or with mutations they were born with, who can't modify their systems, but even in some of those cases, they can halt or slow down further damage.
 

Carl

The Living Force
FOTCM Member
Re: Ketogenic Diet - Path To Transformation?

Laura said:
nicklebleu said:
I just feel that we haven't got to the bottom of all that ... a ketogenic diet surely is a good thing, but seems not to be the end of the story. Seems to me that the issue is a lot more complicated than that. Will do some other test results (TSH and reverse T3 - I am pretty certain I am leptin resistant).
You may change your mind about KD after reading all the papers we are going to get the links to posted. I was going in the direction of thinking "oh, some people MUST need more carbs or this or that" because the whole system and what can go wrong and what probably does go wrong was not clear to me. But, when you put KD together with IF and some resistance training rather like what Gedgaudas describes, to stimulate the upregulation of the "wild mtDNA", it all begins to make sense. Obviously, there are going to be people with such damaged mtDNA or with mutations they were born with, who can't modify their systems, but even in some of those cases, they can halt or slow down further damage.
I have yet to understand exactly what you're talking about in terms of the mechanisms and the "how it works" here, as I haven't yet read in enough detail.

However my personal experience these past couple of days seems to be showing that IF was definitely the missing factor I've been looking for, as I still had periodic brain fog and low energy on an 'impeccable' diet. I was in work until 12AM last night, and I ate at around 7:30PM on my break. It is now 10:30AM. I've had 6 hours sleep, been drinking tea and water all day, and just performed a heavy workout with the weights in my garage.

I feel more alert than usual, and despite having worked out for 30 minutes I feel like I have a lot of energy to go for a run. The thought of food is actually becoming less and less appealing as I continue this short fast, but I plan to eat at around 1PM after doing EE.

It seems we're really onto something here!


Maybe we'll be creating our own stone circles soon enough ;)
 

Laura

Administrator
Administrator
Moderator
FOTCM Member
Re: Ketogenic Diet - Path To Transformation?

Thought I'd try to get some excerpts in and pointers to papers to read.

From: The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism

By: Richard L. Veech, Laboratory of Membrane Biochemistry and Biophysics, National Institutes of Alcoholism and Alcohol Abuse, 12501 Washington Ave., Rockville, MD 20850, USA

Abstract
The effects of ketone body metabolism suggests that mild ketosis may offer therapeutic potential in a variety of different common and rare disease states. These inferences follow directly from the metabolic effects of ketosis and the higher inherent energy present in d-b-hydroxybutyrate relative to pyruvate, the normal mitochondrial fuel produced by glycolysis leading to an increase in the DG0 of ATP hydrolysis. The large categories of disease for which ketones may have therapeutic effects are:

(1) diseases of substrate insufficiency or insulin resistance,
(2) diseases resulting from free radical damage,
(3) disease resulting from hypoxia.

Current ketogenic diets are all characterized by elevations of free fatty acids, which may lead to metabolic inefficiency by activation of the PPARsystem and its associated uncoupling mitochondrial uncoupling proteins. New diets comprised of ketone bodies themselves or their esters may obviate this present difficulty.
Published by Elsevier Ltd.

... How ketone bodies could increase the
hydraulic efficiency of heart by 28% could not be
explained by the changes in the glycolytic pathway
alone, but rather by the changes that were induced
in mitochondrial ATP production by ketone body
metabolism.

...

The fundamental reason why the metabolism of
ketone bodies produce an increase of 28% in the
hydraulic efficiency of heart compared with a heart
metabolizing glucose alone is that there is an inherently
higher heat of combustion in d-b-hydroxybutyrate than
in pyruvate, the mitochondrial substrate which is the
end product of glycolysis (Table 1).
If pyruvate were burned in a bomb calorimeter, it
would liberate 185.7 kcal/mole of C2 units, whereas the
combustion of d-b-hydroxybutyrate would liberate
243.6, or 31% more calories per C2 unit than
pyruvate. Metabolizing d-b-hydroxybutyrate in perfused
working heart creates a 28% increase in the
hydraulic efficiency of heart when compared to the
metabolism of the end product of glycolysis, pyruvate.
The mitochondrial processes of electron transport and
ATP synthesis appear to be capable of capturing this
inherent energy contained in the substrates being
metabolized.

...
Among
the common non-nitrogenous substrates for mitochondrial
energy generation, ketone bodies deserve the
designation of a ‘‘superfuel’’.

...
The metabolic effects of ketone bodies are of
particular relevance to brain metabolism, where Cahill
and his colleagues have established that over 60% of the
metabolic energy needs of brain can be supplied by
ketone bodies, rather than by glucose [11].

...

Although brain has insulin receptors, it has either no
or very low insulin levels making ketosis the only
practical mechanism for increasing the efficiency of
oxidation ATP generation in that organ.
Then, a discussion of Ketogenic diet uses such as:

Refractory Epilepsy
Weight loss
Adjunct to cancer therapies

Feeding a ketogenic diet to mice with implanted tumors
decreased tumor size as well as decreasing muscle
wasting associated with tumor transplantation [34].
Similar results have been reported in human cancer
patients [35,36]. In human patients with advanced
astrocytomas, feeding of a ketogenic diet decreased
tumor glucose uptake and in part of the group an
increase in patient performance [36]. In a surprising
report in mice implanted with astrocytoma, a ketogenic
diet associated with caloric restriction resulted in an
80% decrease in tumor mass and a decrease in tumor
vascularity implying an inhibition of angiogenesis [37].
This part really caught my eye because it is talking about standard IV solutions:

Traditional parenteral fluid therapy as currently
practiced uses fluids whose compositions are historical
and have not been subjected to systematic study of less
toxic alternatives. It has been argued that the use of
acetate in dialysis fluids and racemic d,l-lactate in both
dialysis and parenteral fluid therapy for burns or
resuscitation results in significant and unnecessary
toxicity [38]. A recent report by the Academy of
Medicine suggests a more systematic investigation of
the use of Na d-b-hydroxybutyrate as a replacement of
the conventional anions in parenteral fluid therapy [39].

In response, studies funded by the military have
suggested that resuscitation fluids containing Na d-bhydroxybutyrate
instead of the traditional d,l-lactate
can prevent apoptosis in lung which occurs 24 h after
severe hemorrhage in a rodent model [40]. DaNang lung
was a leading cause of morbidity and mortality in
combat casualties during the Viet Nam war when
resuscitation with large volumes of conventional Ringer’s
lactate became standard therapy. These studies in
animals suggest that fluids containing d,l-lactate are
associated with significant toxic effects which can be
avoided if d-b-hydroxybutyrate replaced the lactate.
Progressive heart block ending in cardiac arrest can be
induced in rats by administration of Na d,l-lactate and
similar forms of heart block are observed in children
receiving up to 20 l of Ringer’s d,l-lactate during the
initial phases of burn therapy [41]. Investigation of the
use of ketone containing fluids would seem indicated.
Used with congenital genetic disorders:

Perhaps the most dramatic therapeutic response to
therapy with Na salts of ketone bodies has been the
report of the response of 3 patients with the rare genetic
disease caused by acyl CoA dehydrogenase deficiency.
This disease is associated with an inability to metabolized
fatty acids by b oxidation lead to leukoencephalopathy
and cardiomyopathy, of which the later form is
more common. It is conventionally treated with a low
fat diet and increased carnitine to bind free fatty acids.
Three patients who became refractory to this therapy
were treated with very small doses in the order of 5 g/day
of Na d,l-b-hydroxybutyrate and all showed dramatic
improvement in cardiac function and in the extent of
leukodystrophy in the brain as judged by MRI [42]. One
patient with quadriplegia showed a clearing of symptoms,
certainly a dramatic response. The l-form of bhydroxybutyrate
is a product of b oxidation, while the
d-form is the product of ketone body synthesis through
HMG CoA. Fatty acid synthesis for myelin production
requires the d-form for fatty acid synthesis, whereas
there would clearly be a deficiency of the l-form in this
genetic condition. Which isomeric form is therapeutic in
this condition is unknown, since the administration of
the d,l-form was dictated purely on the basis of cost of
the material from Sigma, which is dependent not on
inherent cost, but rather on commercial availability.
Regarding diabetes

The excessive production of ketone bodies during
diabetic ketoacidosis is a life threatening condition
usually seen in type I diabetics after some intercurrent
event. It is characterized by profound hyperglycemia
with insulin resistance and elevated blood ketone bodies
approaching 25mM, blood HCO3 approaching 0 and
blood pH approaching 7 causing hyperventilation and a
compensatory low pCO2. Death occurs from the low pH
and vascular collapse secondary to urinary loss of Na+
and K+ in an osmotic diuresis. It is not surprising that
physicians view elevation of blood ketone bodies with
alarm.

However, our data on the acute effects of insulin and
ketone bodies in the perfused working heart suggest that
ketosis, within limits, mimic the acute effects of insulin.
...
Both insulin and ketones
have the same effects on the metabolites of the first third
to the citric acid cycle, on mitochondrial redox states
and both increase the hydraulic efficiency of the working
perfused heart. Viewed in this light, mild ketosis
provides the same metabolic effects as insulin, but at
the metabolic or primitive control level which by-passes
the complex signaling pathway of insulin. During
prolonged fasting, when insulin levels approach 0, mild
ketosis compensates metabolically for the absence of
insulin effects. It follows that the induction of mild
ketosis would be therapeutic in insulin resistant states.

....

A major limitation in achieving ‘‘tight control’’ of
diabetics, is the risk of increased episodes of hypoglycemia.
This consequence of robust insulin therapy is
particularly frequent in type I diabetics. Because of the
potentially serious consequences of cognitive impairment
associated with hypoglycemia, physicians are
reluctant to keep blood glucose within ranges which
are thought to be optimum for the prevention of longterm
vascular disease. Ketone bodies are an alternative
to glucose as a supplier of the metabolic energy needs
for brain. Cahill has shown [51] that during prolonged
fasting, when total blood ketone bodies are in the 5–
7mM range, blood glucose concentrations can be
decreased to below 1mM without either convulsions
or any discernable impairment of cognitive function. At
these concentrations, ketone bodies can provide essentially
all of the energy demands in brain to maintain
function. The induction of mild ketosis therefore offers a
method for obtaining tighter control of blood glucose in
brittle diabetics without the induction of the physiological
consequences of hypoglycemia on cerebral function.
Hypoxic states:

One non-medical use in this category would be the use
of mild ketosis to improve physical performance in
settings where extreme exertion is required. Such
situations would exist in the military when troops are
under extreme combat stress and in certain civilian
settings involving emergency personnel. Extreme exertion
leads not only to exhausting but also to impairment
of cognitive and motor skills under conditions of caloric
restriction [52]. Mild ketosis may offer a way to increase
muscle and brain function without elevation of free fatty
acids which will decrease muscle and cardiac metabolic
efficiency through the induction of mitochondrial
uncoupling protein.

Obvious in this category would be the penumbral
damage in heart after coronary occlusion or in brain
following a stroke. In areas of tissue, where O2 supply is
limited, the provision of ketone bodies might provide
benefit in limiting the area of damage. In a neonatal
rodent model of hypoxia, induction of ketosis has been
reported to limit brain damage in comparison to control
animals after exposure to 3 h of hypoxia [53]. Similar
effects of ketone bodies in limiting the area of brain
damage have been reported in rodent bilateral carotid
occlusion models [54].
Parkinson's

Parkinson’s disease is a common, generally acquired
movement disorder characterized by bradykinesia,
rigidity and tremor resulting from destruction of over
80% of the mesencephalic dopaminergic neurons when
clinical symptoms of the disease appear. Dopaminergic
neurons decline in numbers in all aging humans, but the
rate of destruction is accelerated in patients with clinical
Parkinsonism, with symptoms most commonly appearing
in the 6th decade. It is thought to result from
continued free radical damage to dopaminergic neurons,
which with high iron content, are particularly subject to
this toxicity. The disease is treatable for a time by dopa
administration, but as damage and death of dopaminergic
neurons continues, dopa therapy becomes either
ineffective or limited by its toxicity. Since there is little
genetic loading in this disease, except in the rare early
onset forms, it is clear that non-genetic therapies are
essential.

The major sources of free radical production is the
partially reduced co-enzyme Q semiquinone [18].
...
The metabolism of ketone bodies oxidizes the Q couple and
therefore should decrease the amount of Q semiquinone,
QHd, thereby decreasing free radical production. In
addition the metabolism of ketones, reduces the
cytosolic [NADP+]/[NADPH] couple [43] whose near
equilibrium substrate glutathione is the terminal distructant
of H2O2.
and Alzheimer's

Alzheimer’s disease is a common form of dementia
affecting 3% of those 65–74 years old, 18.7% of those
75–84, and 47.2% of those over 85 years of age [63].
Approximately 20–30% of Alzheimer’s disease results in
defects in 6 different genes. Defects in chromosome 1
and 14, encoding presenilin 1 and 2; in chromosome 21,
encoding amyloid precursor protein, lead to early onset
Alzheimer’s disease. Defects in chromosome 21, encoding
a2 microglobulin; or in chromosome 19, encoding
apolipoprotein E is associated with late onset Alzheimer’s
disease. All of the genetic defects result in
excessive accumulation of amyloid protein. The remaining
70–80% of Alzheimer’s disease have the same
pathological findings of amyloid plaques, phosphorylated
microtubular proteins and loss of hippocampal
neurons associated with memory loss and increasing
dementia, but from causes which include ischemia [64]
mild trauma [65] elevated plasma homocystine [66]
insulin resistance [67] and impaired brain energy
metabolism [68]. The clinical phenotype of Alzheimer’s
disease is clearly a complex multifactoral disease.

A major finding in Alzheimer’s disease is the decrease
in brain acetyl choline [69]. This finding has led to the
widespread use of acetyl cholinesterase inhibitor in the
treatment of the disease, but with only very limited if
any improvement [70]. However this pharmacological
approach fails to address the underlying pathophysiology
of the disease. The common feature of Alzheimer’s
disease is the elevated levels of proteolytic fragments of
b amyloid both extra and intracellularly [71]. It is
reported that the 1–42 fragment of b amyloid, Ab142,
stimulates a mitochondrial isoform of glycogen synthase
kinase 3b [72] which phosphorylates and inactivates the
pyruvate dehydrogenase multienzyme complex [73] and
results in the decrease in acetyl choline synthesis [74]
characteristic of the Alzheimer’s disease phenotype.
Since under normal conditions brain is entirely dependent
on glucose as an energy source, inhibition of PDH
would be expected to decrease mitochondrial acetyl
CoA formation and hence citrate formation, a necessary
precursor of acetyl choline. Blockade of PDH is
characteristic of insulin lack in heart and ketone bodies
are the physiological mechanism which overcomes this
inhibition. If this were to occur in neurons, administration
of ketone bodies should by-pass this block. We
tested this hypothesis in primary rat hippocampal
neuronal cultures exposed to 5 mM Ab142 and found
that the addition of 4mM Na d-b-hydroxybutyrate
protected against Ab142 toxicity [62]. Induction of mild
ketosis would therefore seem a reasonable potential
therapy in Alzheimer’s disease.
Methods of Induction of Ketosis

Mild ketosis can be induced in man by either
prolonged fasting or by feeding a high fat, low
carbohydrate diet. Total starvation is not a therapeutic
option, since death results in a normal weight man in
68–72 days.

Oral administration of Na d,l-b-hydroxybutyrate in
doses from 80 to 900 mg/kg/day was sufficient to achieve
peak blood levels of total d-b-hydroxybutyrate+acetoacetate
of 0.19–0.36mM producing a therapeutic
response in children with acyl CoA dehydrogenase
deficiency [42]. In a 70 kg man to achieve these levels
of ketosis would require the feeding of between 5.6 to
63 g/day at a present cost of $3 g1 or $17 to $189 day1.
...

the present costs of the administration of salts of
d-b-hydroxybutyrate to achieve ketosis makes this
approach unlikely.
So, that's it for that paper. Note that this was back in 2003.
 

Laura

Administrator
Administrator
Moderator
FOTCM Member
Re: Ketogenic Diet - Path To Transformation?

Next paper:

The ketogenic diet as a treatment paradigm for diverse neurological disorders

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321471/

Carl E. Stafstrom1,2 and Jong M. Rho3,4*
1 Department of Neurology, University of Wisconsin, Madison, WI, USA
2 Department of Pediatrics University of Wisconsin, Madison, WI, USA
3 Department of Pediatrics, University of Calgary Faculty of Medicine, Calgary, AB, Canada
4 Department of Clinical Neurosciences, University of Calgary Faculty of Medicine, Calgary, AB, Canada

This one will not copy/paste anywhere but there is a bit I'm going to try to fix up here:

As mentioned above, given the growing evidence that the KD
enhances mitochondrial functioning and biogenesis (Boughetal.,
2006; Maaloufetal., 2009; Kimdoetal., 2010), it is logical
to ask whether patients with known mitochondrial cytopathies
might derive a benefit from the KD and/or ketone bodies such
as BHB. At the same time, it must be considered that inher-
ent mitochondrial dysfunction might predispose individuals to
adverse toxicities from high fatty acid loads that could overwhelm
β-oxidation within the mitochondrial matrix. Experimental data
described above attest to significant improvements in mitochon-
drial function, and many lines of evidence point to the rationale
of therapeutically targeting mitochondrial bioenergetics for other
disease states (Wallaceetal.,2010), but is there any clinical evi-
dence in patients with intrinsic mitochondrial disorders? Kang
et al.(2007) reported that the KD was both safe and effective
in 14 pediatric patients with established mitochondrial defects
in complexes I, II, and IV, all of whom had medically intractable
epilepsy. These authors observed that half of these patients became
seizure-free on the KD, and only four patients failed to respond.

Hence, these preliminary data suggest that the KD is not necessarily
contraindicated in patients with mitochondrial respiratory chain
abnormalities.
Note that the standard Ketogenic Diet includes such things as cheese and cream, so one wonders, of course, if these experiments would have been nearly 100% successful if they had eliminated dairy from the diet list.
 

Laura

Administrator
Administrator
Moderator
FOTCM Member
Re: Ketogenic Diet - Path To Transformation?

Next one: (Another that doesn't want to behave with copy/paste.)

The nervous system and metabolic dysregulation: emerging evidence converges on ketogenic diet therapy

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3312079/

David N. Ruskin and Susan A. Masino*
Neuroscience Program, Department of Psychology, Trinity College, Hartford, CT, USA

It's worth reading for some of the science and the emphasis on brain function in relation to metabolism. Geeze, for those with challenged metabolism, how much better MIGHT our brains work?
 
Top Bottom