A photo of my little girl Chouette who is now 23 years old which is equivalent to 110 years for humans.
Like all my pets over many decades I have had Chouette on a high quality diet and supplement program which keeps her going.
Last year at the Vet we had to do some blood work on her and the Vet was shocked because her blood work was what they would expect in a cat half her age.
I use these same principles when I am working with clients to help them to reverse their Biological Age.
Pricera our NAD+ precursor formulation is now available!
Why maintaining optimal NAD+ levels as we age is critical to our quality of life, healthspan and potentially lifespan
I wanted to share with you today why I believe that maintaining optimal NAD+ levels is critical for healthy aging, extending healthspan – and potentially lifespan (as has been shown in animal studies).
“In my opinion, NAD therapy will turn out to be one of the greatest advances in medical science since Fleming developed penicillin”.
Dr. Phil Milgram, MD
NAD+ levels decrease with age:
People aged 50 have about 40% less NAD+
By the age of 80 years, NAD+ levels decline between 90-98%
NAD+ and the Sirtuin Longevity Genes
Optimal NAD+ levels are critical for the activation of the Sirtuin longevity genes.
Limited Sirtuin longevity gene activity can lead to an acceleration of the aging process: one example of this is vascular aging.
Vascular aging is responsible for a constellation of disorders, such as cardiac and neurologic conditions, muscle loss, impaired wound healing and overall frailty, amongst others.
Multiple animal studies have demonstrated that increasing sirtuin activity leads to:
•Longer life •Less age-related loss of function •Less DNA damage
NAD+ maintains and builds sirtuin levels and activity
Exercise Performance
Another impressive benefit of optimizing NAD+ levels is in the area of exercise:
In a mouse study, the cohort which was supplemented to optimize NAD+ levels it increased their exercise capacity between 56 and 80 percent, compared with untreated mice.
David Sinclair, PhD commented about the results of this study:
“Even if you’re an athlete, you eventually decline,” Sinclair said. “But there is another category of people—what about those who are in a wheelchair or those with otherwise reduced mobility?”
In another study involving elderly men, supplementation with an NAD+ precursor resulted in improved exercise performance:
The men in this study had an 8% improvement in peak isometric muscle torque (a measure of muscle force) and a 15% improvement in fatigue associated with exercise.
Other Research Highlights:
• Boosting NAD+ biosynthesis by using key NAD+ intermediates is now drawing significant attention for: Alzheimer’s/Type 2 Diabetes/Heart Failure/ Hearing Loss • NAD+ precursors have been shown to increase stem cell colonies by 75% in the gut of aging mice • Other studies point to the role of NAD+ in restoring circadian rhythms needed for restorative sleep • SirT1 overexpression protects against Alzheimer’s and Huntington’s disease as well as ALS
Low NAD+ Levels Can Contribute to the Following:
•Accelerates aging •Increases sunburn and skin cancer •Decreases cellular antioxidants •Decreases metabolism along with thyroid hormones •Harms immune function •Increases inflammation •Impairs brain function •Can cause hypoxia intracellularly •Associated with Chronic Fatigue Syndrome •May worsen weight gain and metabolic syndrome •May worsen cardiovascular diseases May contribute to MS (multiple sclerosis)
Why Is It Important to Increase NAD+ Levels?
General Benefits
•Low NAD+ levels can accelerate the aging process •NAD+ is vital for mitochondrial health •NAD+ plays a key role in cellular metabolism and energy production •NAD+ is a rate-limiting co-substrate for sirtuins •High NAD+ levels are essential for DNA repair and recovery •NAD+ activates CD38, which is present on many immune cells (white blood cells) and associated with impaired immune responses. •Enhances autophagy •Helps maintain redox potential
Specific Conditions
•Positive impact on the Diabesity Spectrum •Low NAD+ levels may worsen cardiovascular diseases •Low NAD+ levels may increase inflammation
In my opinion, you cannot age well and extend healthspan without addressing and maximizing NAD+ levels, especially with older patients.
For more information about Pricera or where you can get some reach out to me.
In our continuing series on compounds that can have a positive
impact on prevention of viral infections as well as improving response to
infections today I want to highlight Vitamin D.
Vitamin D not only acts as a vitamin but also as a prohormone and
it influences hundreds of biochemical processes in human physiology.
Following is a press release from the Orthomolecular Medicine News
Service which provides details on how Vitamin D could reduce the risk of
influenza and COVID-19 infection and death.
(OMNS Apr 9,
2020) There are two main reasons why respiratory tract infections such as
influenza and COVID-19 occur in winter: winter sun and weather and low vitamin
D status. Many viruses live longer outside the body when sunlight, temperature,
and humidity levels are low as they are in winter [1].Vitamin D is an important component of the
body’s immune system, and it is low in winter due to low solar ultraviolet-B
(UVB) doses from exposure and the low supplement intakes of most. While nothing
can be done about winter sun and weather, vitamin D status can be raised
through vitamin D supplements.
Vitamin D has
several mechanisms that can reduce risk of infections [2]. Important mechanisms regarding respiratory
tract infections include:
inducing production of cathelicidins and defensins that can lower viral survival and replication rates as well as reduce risk of bacterial infection
reducing the cytokine storm that causes inflammation and damage to the lining of the lungs that can lead to pneumonia and acute respiratory distress syndrome.
Vitamin D deficiency has been found to contribute to acute respiratory distress syndrome, a major cause of death associated with COVID-19 [3]. An analysis of case-fatality rates in 12 U.S. communities during the 1918-1919 influenza pandemic found that communities in the sunny south and west had much lower case-fatality rates (generally from pneumonia) than those in the darker northeast [4].
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.
