People who live with depression have low blood levels of a specific molecule, new medical research has revealed. It’s called acetyl-L-carnitine, and those with particularly severe, treatment-resistant or childhood onset depression were found to have the lowest levels.
Naturally produced by the body, acetyl-L-carnitine plays a crucial
role in metabolising fat and the production of energy. It’s also widely
available as a dietary supplement – not some strange and esoteric thing.
Now
researchers from multiple institutions have found a link to depression,
noticing a clear correlation between the condition and noticeably low
levels of acetyl-L-carnitine.
In recent years, more and more
evidence has been building to suggest this link. Since at least 1991,
medical researchers have been aware of acetyl-L-carnitine’s potential to
treat depression, particularly in geriatric and comorbid patients, with the substance showing greater efficacy than a placebo.
More recently, Carla Nasca of the Rockefeller University led a study on rodents,
which found that acetyl-L-carnitine had a fast-acting antidepressant
effect on rats, kicking into effect in just a few days, rather than the
weeks it takes for drugs like SSRIs.
Now Nasca and colleagues have conducted a study on human patients to see if there’s a basis for a similar trial in people.
“It’s the number one reason for absenteeism at work, and one of
the leading causes of suicide. Worse, current pharmacological
treatments are effective for only about 50 percent of the people for
whom they’re prescribed. And they have numerous side effects, often
decreasing long term compliance.”
The research team recruited 71
patients with a diagnosis of depression. These were men and women, aged
between 20 and 70. They also recruited 45 demographically matched
healthy controls.
The patients had to fill out a detailed
questionnaire, undergo a clinical assessment and medical history, and
give a blood sample. Of the patients with depression, 28 had moderate
depression and 43 had severe depression at the time of the study.
When
compared to the age- and sex-matched healthy controls, the patients
with depression had substantially lower levels of acetyl-L-carnitine.
Those
with the most severe depression had the lowest levels. This included
patients whose depression had resisted antidepressant drugs, those with
early onset, and those who had experienced childhood abuse, neglect,
poverty or violence.
These patients constitute around 25-30
percent of all people suffering depression, and are the most in need of
help, the researchers said.
But there are a few steps to be done before acetyl-L-carnitine
supplements can be approved as a treatment. In particular, clinical
trials on human patients with depression, since, as we know, results from rodent models can’t always be replicated in humans.
The
researchers also don’t know the reason for the correlation, or the
effect it has. The rat research suggests that acetyl-L-carnitine plays a
role in the brain, preventing the excessive firing of excitatory
neurons, but this will need to be explored further as well.
“We’ve identified an important new biomarker of major depression disorder,” Rasgon said.
“We
didn’t test whether supplementing with that substance could actually
improve patients’ symptoms. What’s the appropriate dose, frequency,
duration? We need to answer many questions before proceeding with
recommendations, yet. This is the first step toward developing that
knowledge, which will require large-scale, carefully controlled clinical
trials.”
And we’ll be eagerly awaiting the results of those trials.
Meanwhile, the team’s research can be found in the journal PNAS.
Dietary intervention restores protective protein and decreases death rate in mice
Source: Society for Neuroscience
The incidence of dementia and Alzheimer’s continues to escalate in the general population.
LCHF/Keto diets have proven to be beneficial to individuals dealing with these health issues.
It has been suggested that these conditions may partly be due to impaired glucose metabolism in the brain, hence the increasing use of the term “Type 3 Diabetes”.
Enabling the brain to use ketones for its energy source therefore can provide some benefit with regards to brain function.
A major challenge with this is that a radical dietary shift in the geriatric population can be quite challenging – if not impossible.
Usage of exogenous ketone compounds is one potential option in this situation.
Following is an article from Science Daily which talks about published research which suggests that increasing ketone levels in the diet can help to protect neurons from death during the progression of Alzheimer’s disease.
Summary: A ketone-supplemented diet may protect neurons from death during the progression of Alzheimer’s disease, according to research in mice.
A
ketone-supplemented diet may protect neurons from death during the
progression of Alzheimer’s disease, according to research in mice
recently published in JNeurosci.
Early in the development of Alzheimer’s
disease, the brain becomes over excited, potentially through the loss of
inhibitory, or GABAergic, interneurons that keep other neurons from
signaling too much. Because interneurons require more energy compared to
other neurons, they may be more susceptible to dying when they
encounter the Alzheimer’s disease protein amyloid beta. Amyloid beta has
been shown to damage mitochondria — the metabolic engine for cells —
by interfering with SIRT3, a protein that preserves mitochondrial
functions and protects neurons.
Cheng et al. genetically reduced levels
of SIRT3 in mouse models of Alzheimer’s disease. Mice with low levels of
SIRT3 experienced a much higher mortality rate, more violent seizures,
and increased interneuron death compared to the mice from the standard
Alzheimer’s disease model and control mice. However, the mice with
reduced levels of SIRT3 experienced fewer seizures and were less likely
to die when they ate a diet rich in ketones, a specific type of fatty
acid. The diet also increased levels of SIRT3 in the mice.
Increasing SIRT3 levels via ketone
consumption may be a way to protect interneurons and delay the
progression of Alzheimer’s disease.
Story Source:
Materials provided by Society for Neuroscience. Note: Content may be edited for style and length.
Journal Reference:
Aiwu Cheng, Jing Wang, Nathaniel Ghena,
Qijin Zhao, Isabella Perone, M. Todd King, Richard L. Veech, Myriam
Gorospe, Ruiqian Wan, Mark P. Mattson. SIRT3 Haploinsufficiency
Aggravates Loss of GABAergic Interneurons and Neuronal Network
Hyperexcitability in an Alzheimer’s Disease Model. The Journal of Neuroscience, 2019; 1446-19 DOI: 10.1523/JNEUROSCI.1446-19.2019
Abstract
SIRT3 Haploinsufficiency
Aggravates Loss of GABAergic Interneurons and Neuronal Network
Hyperexcitability in an Alzheimer’s Disease Model
Impaired mitochondrial function and
aberrant neuronal network activity are believed to be early events in
the pathogenesis of Alzheimer’s disease (AD), but how mitochondrial
alterations contribute to aberrant activity in neuronal circuits is
unknown. In this study, we examined the function of mitochondrial
protein deacetylase sirtuin 3 (SIRT3) in the pathogenesis of AD.
Compared to AppPs1 mice, Sirt3-haploinsufficient AppPs1 mice
(Sirt3+/-AppPs1) exhibit early epileptiform EEG activity and Seizure.
Both male and female Sirt3+/-AppPs1 mice were observed to die
prematurely before five months of age.
When comparing male mice among different genotypes, Sirt3
haploinsufficiency renders GABAergic interneurons in the cerebral cortex
vulnerable to degeneration and associated neuronal network
hyperexcitability. Feeding Sirt3+/-AppPs1 AD mice with a ketone
ester-rich diet increases SIRT3 expression and prevents seizure-related
death and the degeneration of GABAergic neurons, indicating that the
aggravated GABAergic neuron loss and neuronal network hyperexcitability
in Sirt3+/-AppPs1 mice are caused by SIRT3 reduction and can be rescued
by increase of SIRT3 expression. Consistent with a protective role in
AD, SIRT3 levels are reduced in association with cerebral cortical Aβ
pathology in AD patients. In summary, SIRT3 preserves GABAergic
interneurons and protects cerebral circuits against hyperexcitability,
and this neuroprotective mechanism can be bolstered by dietary ketone
esters.
SIGNIFICANCE STATEMENT
GABAergic neurons provide the main
inhibitory control of neuronal activity in the brain. By preserving
mitochondrial function, SIRT3 protects parvalbumin and calretinin
interneurons against Aβ-associated dysfunction and degeneration in
AppPs1 AD mice, thus restraining neuronal network hyperactivity. The
neuronal network dysfunction that occurs in AD can be partially reversed
by physiological, dietary, and pharmacological interventions to
increase SIRT3 expression and enhance the functionality of GABAergic
interneurons.
Fasting in its many forms can provide profound beneficial health benefits.
Following is an article on this topic authored by Dr. Dan Pompa which provides a good overview.
Regards,
Robert (Rob) Lamberton
Fasting is a very old ritual to boost health that is found in religions all over the world and is rooted in natural ancestral cycles of feast and famine. Before we had grocery stores, restaurants, and even food delivery services- there were often times with very little to no food. Following times of famine, there was an abundance of food (following a successful harvest, forage, or hunt). Even animal wisdom harnesses the power of fasting- like dogs, that will intuitively stop eating when they are sick. More and more studies are emerging on the incredible benefits that fasting can have, on not only for health but also suggesting a boost in longevity.
Fasting diets
have nothing to do with WHAT or HOW MUCH you eat, but WHEN you eat.
Intermittent fasting (or IF) is the art of restricted time eating, so instead
of counting calories or restricting what types of foods you eat- the entire
“diet” relies on when you do, and don’t eat.
Recent Research on Fasting
Have Your Cake And Eat It Too: Boost Health
and Longevity Not By Changing What You Eat, But When You
Eat.
Intermittent Fasting Research
Although Intermittent Fasting to boost health has gained
popularity in more recent years, its wisdom dates back to our ancestors from
the stone age. Apart from periods of feast and famine, our ancestors’ lives
were also heavily dictated by the rising and setting of the sun; activities
like eating naturally happened during day time. Our exposure to light, food,
and movement are the main tenets that inform and program our circadian rhythm.
This internal rhythm influences everything from sleep-wake cycles, hormone
release, eating habits and digestion, body temperature, and other important
bodily functions.1 Intermittent fasting plays a role in giving the
body an adequate period of rest from digestion, enabling it to not only heal-
but thrive.
Research on Fasting is Extensive
Many of the
studies regarding fasting to boost health and longevity have been done on
animals. However, these studies suggest promising effects on metabolic
functions, health, and lifespan for humans. Although there are many variables,
Rafael deCabo, a scientist at the National Institute on Aging and the
study’s lead author explains that;
“in the absence of
calorie restriction, and independent of diet composition, fasting mice do
better than non-fasting”.2
Boost Health! The ever-increasing research
regarding fasting suggests some incredible health and longevity benefits
including:
Autophagy
A boost in stem cells
Boost in ketones
Hormone optimization
Increased insulin sensitivity
Reset of the microbiome
Reset of the DNA (gene code)
Decrease in inflammation
A decrease in oxidative stress
Reduced instances of chronic disease and obesity
Protection against unusual deterioration of cognitive function
Fat loss
Cancer prevention
Promotion of better sleep
More satiety/ reduced hunger
Although benefits
are often examined as individual points, they are in fact very much intertwined
to promote overall longevity. One of the main ways IF leads to longevity is
“multi-system regeneration,” which fasting researcher Dr. Valter Longo explains
occurs during the presence of ketones in the blood. The autophagy process that
happens during a fasting period breaks down weak and damaged cells, which are
then replaced with new stem cells after food is reintroduced.
“You get rid of
the junk during starvation — and once you have food, you can rebuild… The
damaged cells are replaced with new cells, working cells — and now the system
starts working properly.”
Research on Fasting: Health and Longevity
All these
benefits suggest a direct link between fasting and longevity, although
conducting a clinical longevity study in humans is unfeasible at the moment,
for would cost “a hundred million dollars or more,” according to Longo. “But if
you look at the data from our trial … it would be hard to see how they would
not live longer.”
Dr. Valter Longo
and Dr. Satchin Panda’s study demonstrated that a 12-hour feeding window
reduced blood cholesterol, fasting blood sugar, body weight, body fat,
inflammation, and dysbiosis, and increased energy expenditure, motor control,
endurance, sleep, and cardiac function.3 Their study examined the
intricate relationship between time-restricted feeding (IF), circadian health,
and ultimately concluded that simply limiting your eating window to a minimum
of 12 hours reduces biological age irrelevant of any dietary changes! Indeed,
their study suggests that you can have your cake and eat it too… so long as you
do so within your eating window.
Research on Fasting: How To Do It
There are many
different fasting styles that range from multiple days water-only fasts, to
bone broth fasts, to alternate day fasting… but intermittent fasting itself is
conceptually incredibly simple: engage in a particular restricted eating
window, preferably rooted in 2 meals (and no snacking). This might seem not too
far off from your current habits, but studies show the average American eats
17-21 times a day! This is detrimental to our health and longevity.
Classic Intermittent Fasting: The Eating
Window
The key is,
aforementioned, restricting your eating window. The science suggests a very minimum
of 12 hours to see any benefits, so if you have no experience fasting- start
there. If you eat your first meal at 8 am, no food (or beverage other than
plain water) after 8 pm.4 From there, extend the fasting window to
ideally (at least) 16 hours. Whether you decide to skip breakfast or dinner is
completely personal, find what works best for your schedule and which option is
more sustainable over the long run. A 2018 study comparing a 12-hour feeding
window to an 8-hour feeding window demonstrated that although both groups lost
weight, those in the 8-hour feeding window group dramatically lower insulin
levels, improved insulin sensitivity, and significantly lower blood pressure in
only five weeks.5
Research on Fasting: One Meal a Day
“One meal a day”
(or OMAD) is an extreme version of intermittent fasting. An individual shortens
their eating window to essentially the duration of one single meal. The
benefits of this technique essentially amplify all the aforementioned benefits
of a 16/8 IF protocol. OMAD gives the body even more time in this resting
(vs. digesting) state. OMAD is not, however, for everyone- nor should it be the
goal. Consuming one meal a day can be more taxing on the adrenal system. OMAD
could even induce more detoxification than an individual can handle at once.
Like any type of
good stress (exercise, sauna, cold therapy), the adrenals and overall system
need to be strong enough to withstand the short term stressor. Ease into
intermittent fasting at your own pace, and always listen to your body. A great
way to transition into it and/ or reboot your system is to take part in the
5-day Fasting Mimicking Diet™.
Research on Fasting to Boost Health and
Longevity: The Fasting Mimicking DietTM
Fasting for health and longevity can be a daunting endeavor for someone who is used to eating 3+ meals a day their entire lives, and this is where the fasting mimicking diet comes in. Fasting expert and researcher Dr. Valter Longo created the Fasting Mimicking Diet program that mimics the benefits of a fasting protocol, combining both the benefits of intermittent fasting and a longer term fast (through caloric restriction). Prolon® takes out the guesswork but providing clients with all their meals for a 5 day period. Longo is the Director of both the Longevity Institute at the University of Southern California and The Program on Longevity and Cancer at IFOM in Milan, and his clinical study demonstrated remarkable benefits that fasting has to offer in just 5 days (repeated for 3 months):
Promote stem cell-based renewal in the body
Decrease excess body fat while preserving lean muscle mass
Maintain healthy levels of blood glucose, cholesterol, & blood pressure
Decreased hormone IGF-1 (which has been implicated with aging and disease)6
We suggest using
this fasting
mimicking diet to boost health if you are completely new to fasting
or are trying to break destructive eating patterns! This can be a bridge to
continue on with regular Intermittent Fasting thereafter!
References
Longo, Valter D., and Satchidananda Panda. “Fasting, Circadian Rhythms, and Time-Restricted Feeding in Healthy Lifespan.” Cell Metabolism, vol. 23, no. 6, 2016, pp. 1048–1059., doi:10.1016/j.cmet.2016.06.001.
Mitchell, Sarah J., et al. “Daily Fasting Improves Health and Survival in Male Mice Independent of Diet Composition and Calories.” Cell Metabolism, vol. 29, no. 1, Jan. 2019, doi:10.1016/j.cmet.2018.08.011
Sutton, Elizabeth F., et al. “Early Time-Restricted Feeding Improves Insulin Sensitivity, Blood Pressure, and Oxidative Stress Even without Weight Loss in Men with Prediabetes.” Cell Metabolism, vol. 27, no. 6, 2018, doi:10.1016/j.cmet.2018.04.010.
Wei, Min, et al. “Fasting-Mimicking Diet and Markers/Risk Factors for Aging, Diabetes, Cancer, and Cardiovascular Disease.” Science Translational Medicine, vol. 9, no. 377, 2017, doi:10.1126/scitranslmed.aai8700.
We love sweet treats. But too much sugar in our diets can lead to weight gain and obesity, Type 2 diabetes and dental decay. We know we shouldn’t be eating candy, ice cream, cookies, cakes and drinking sugary sodas, but sometimes they are so hard to resist.
It’s as if our brain is hardwired to want these foods.
As a neuroscientist my research centres on how modern day “obesogenic”, or obesity-promoting, diets
change the brain. I want to understand how what we eat alters our
behaviour and whether brain changes can be mitigated by other lifestyle
factors.
Your body runs on sugar – glucose to be precise. Glucose comes from the Greek word glukos which means sweet. Glucose fuels the cells that make up our body – including brain cells (neurons).
Dopamine “hits” from eating sugar
On
an evolutionary basis, our primitive ancestors were scavengers. Sugary
foods are excellent sources of energy, so we have evolved to find sweet
foods particularly pleasurable. Foods with unpleasant, bitter and sour
tastes can be unripe, poisonous or rotting – causing sickness.
So
to maximize our survival as a species, we have an innate brain system
that makes us like sweet foods since they’re a great source of energy to
fuel our bodies.
When we eat sweet foods the brain’s reward system – called the mesolimbic dopamine system – gets activated. Dopamine
is a brain chemical released by neurons and can signal that an event
was positive. When the reward system fires, it reinforces behaviours –
making it more likely for us to carry out these actions again.
Dopamine “hits” from eating sugar promote rapid learning to preferentially find more of these foods.
Our
environment today is abundant with sweet, energy rich foods. We no
longer have to forage for these special sugary foods – they are
available everywhere.
Unfortunately, our brain is still
functionally very similar to our ancestors, and it really likes sugar.
So what happens in the brain when we excessively consume sugar?
Can sugar rewire the brain?
The brain continuously remodels and rewires itself through a process called neuroplasticity.
This rewiring can happen in the reward system. Repeated activation of
the reward pathway by drugs or by eating lots of sugary foods causes the
brain to adapt to frequent stimulation, leading to a sort of tolerance.
In the case of sweet foods, this means we need to eat more to get the same rewarding feeling – a classic feature of addiction.
Food addiction
is a controversial subject among scientists and clinicians. While it is
true that you can become physically dependent on certain drugs, it is
debated whether you can be addicted to food when you need it for basic survival.
The brain wants sugar, then more sugar
Regardless of
our need for food to power our bodies, many people experience food
cravings, particularly when stressed, hungry or just faced with an
alluring display of cakes in a coffee shop.
To resist cravings, we
need to inhibit our natural response to indulge in these tasty foods. A
network of inhibitory neurons is critical for controlling behaviour.
These neurons are concentrated in the prefrontal cortex – a key area of the brain involved in decision-making, impulse control and delaying gratification.
Importantly,
this shows that what we eat can influence our ability to resist
temptations and may underlie why diet changes are so difficult for
people.
Importantly,
the brain’s neuroplasticity capabilities allow it to reset to an extent
following cutting down on dietary sugar, and physical exercise can augment this process.
Foods rich in omaga-3 fats (found in fish oil, nuts and seeds) are also
neuroprotective and can boost brain chemicals needed to form new
neurons.
While it’s not easy to break habits like always eating
dessert or making your coffee a double-double, your brain will thank you
for making positive steps.
The first step is often the hardest. These diet changes can often get easier along the way.
Both the U.S. and Canadian governments have been reluctant to include the LCHF (low carb, high fat)/Keto diet as an acceptable option for the populations in both countries.
We recently experienced this here in Canada when the Canadian government revised the Canada food guidelines and despite a significant lobbying effort by researchers, clinicians and the general public they chose to not include the LCHF/Keto diet.
Now in the U.S. a coalition of stakeholders has formed to lobby the U.S. government to include the LCHF/Keto diet in its recommendations.
This group of stakeholders includes researchers, clinicians and members of the general public.
It is only a matter of time before both governments incorporate the LCHF/Keto diet into their recommendations.
There is no one diet that works for everyone but there is no denying the considerable research that has been published on the health benefits of the LCHF/Keto diets, including weight management, potential reversal of Type 2 Diabetes, dementia and Alzheimer’s and many more.
A new group called the Low-Carb Action Network (LCAN), a coalition of
doctors, academics, and average Americans with personal success stories
using low-carb diets, has launched to urge U.S. nutrition leaders to
include a true low-carb diet as part of the 2020 Dietary Guidelines for
Americans (DGA).
LCAN members point to a large and rapidly growing body of
strong scientific research showing carbohydrate restriction to be a safe
and effective strategy to prevent and even reverse chronic,
diet-related conditions such as pre-diabetes/type 2 diabetes,
overweight/obesity and high blood pressure along with a broad array of
other cardiovascular risk factors.
The American Diabetes Association (ADA) recently endorsed
low-carb/keto diets as a standard of care for the prevention and
management of type 2 diabetes, stating that the diet lowers blood
pressure, controls blood sugar, lowers triglycerides (fatty acids in the
blood), raises the “good” cholesterol (HDL-C), and reduces the need for
medication use.
However, the DGA does not include a low-carb diet. For the 2015 DGA,
USDA-HHS ignored some 70 clinical trials demonstrating the effectiveness
of low-carb diets. LCAN does not want important scientific evidence to
again be ignored.
LCAN members are also concerned that USDA (U.S. Department of
Agriculture), in its current scientific reviews, is using an inaccurate
definition of the diet that is not up-to-date with current science and
will lead to misleading, untrustworthy results. Specifically, USDA is
defining “low-carb” as 45 percent of total calories or less, when
leaders in the field agree this number should be 25 percent.
Dr. Eric Westman, associate professor of medicine at Duke
University emphasized that the current dietary guidelines do not apply
to most Americans and that a variety of dietary options should be
presented to the American people, including a low-carbohydrate diet.“One
size does not fit all. If there is anything we’ve learned over the last
four years, it’s that the low-carb approach should be a viable option,”
he stated.
Dr. Mark Cucuzzella, professor of Family Medicine at West Virginia
University added that a a majority of the patients he treats daily have
obesity and “metabolic syndrome,” a combination of conditions driven by
hyperinsulinemia that increase the risk of heart disease, stroke and
diabetes.
“If the government has any responsibility to give advice on nutrition
it should be focused on those who have a medical condition which is
impacted by nutrition and provide evidence-based nutrition solutions,
one being a low-carb diet. This diet is highly effective to prevent and
treat diet-related illnesses and has decades of evidence to support it.
A study conducted last year by the University of North Carolina at
Chapel concluded that only 12 percent of American adults are
metabolically healthy, while 88 percent are on the way to developing
type 2 diabetes, cardiovascular disease or another chronic, diet-related
condition.
Dr. Nadir Ali, chairman, department of cardiology, Clear Lake
Regional Medical Center, and research professor, Department of Nutrition
and Applied Science, University of Houston in Texas, has significant
experience in the science and practice of low-carb diets.
“As a cardiologist, I regularly prescribe a low-carb diet to treat
patients with type 2 diabetes and other heart-related diseases to better
their health and improve their quality of life,” said Dr. Ali. “Given
the significant amount of scientific research and evidence supporting
this diet, it’s time for U.S. nutrition policy leaders to prescribe a
low-carb option for those who are tipping into obesity, diabetes, high
blood pressure and more.”
LCAN plans to launch a grassroots campaign in the coming months to
urge leaders at USDA and HHS to ensure that a properly defined low-carb
diet is included in the DGA to provide a dietary option for the majority
of Americans who suffer from diet-related, chronic diseases. The
next meeting of the Dietary Guidelines Advisory Committee will be held
next month in Houston.
Dietary intervention restores protective protein and decreases death rate in mice
Date: December 9, 2019 Source: Society for Neuroscience Summary:
A ketone-supplemented diet may protect neurons from death during the progression of Alzheimer’s disease, according to research in mice.
I am a big proponent of LCHF (low carb, high fat)/ketogenic diets – this diet has worked well for myself and I have seen it provide many significant benefits in clients I work with.
No one diet will work for everyone however LCHF diets can be extremely beneficial – if not followed continuously then periodically almost like one would do a detox program.
This study suggests that consumption of ketones may be protective against the progression of Alzheimer’s.
A ketone-supplemented diet may protect neurons from death during the progression of Alzheimer’s disease, according to research in mice recently published in JNeurosci.
Early in the development of Alzheimer’s disease, the brain becomes over excited, potentially through the loss of inhibitory, or GABAergic, interneurons that keep other neurons from signaling too much. Because interneurons require more energy compared to other neurons, they may be more susceptible to dying when they encounter the Alzheimer’s disease protein amyloid beta. Amyloid beta has been shown to damage mitochondria — the metabolic engine for cells — by interfering with SIRT3, a protein that preserves mitochondrial functions and protects neurons.
Cheng et al. genetically reduced levels of SIRT3 in mouse models of Alzheimer’s disease. Mice with low levels of SIRT3 experienced a much higher mortality rate, more violent seizures, and increased interneuron death compared to the mice from the standard Alzheimer’s disease model and control mice. However, the mice with reduced levels of SIRT3 experienced fewer seizures and were less likely to die when they ate a diet rich in ketones, a specific type of fatty acid. The diet also increased levels of SIRT3 in the mice.
Increasing SIRT3 levels via ketone consumption may be a way to protect interneurons and delay the progression of Alzheimer’s disease.
Story Source:
Materials provided by Society for Neuroscience. Note: Content may be edited for style and length.
Journal Reference:
Aiwu Cheng, Jing Wang, Nathaniel Ghena, Qijin Zhao, Isabella Perone, M. Todd King, Richard L. Veech, Myriam Gorospe, Ruiqian Wan, Mark P. Mattson. SIRT3 Haploinsufficiency Aggravates Loss of GABAergic Interneurons and Neuronal Network Hyperexcitability in an Alzheimer’s Disease Model. The Journal of Neuroscience, 2019; 1446-19 DOI: 10.1523/JNEUROSCI.1446-19.2019
