Mitochondria Activation and Metabolism:

Burning Fat More Efficiently

Anthony Capasso, MD

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 What do mitochondria have to do with
increasing your energy, weight loss, endurance
and slowing aging?
 Mitochondria

 100000 trillion in your body

 Each one contains thousands of pathways to produce ATP
 Utilize 90% of the oxygen we breathe in.
 They produce energy in the form of ATP from glucose or Fatty acids
 Involved with steroid synthesis (E & T), Lipid metabolism, glucose
metabolism , and cellular calcium metabolism.
 5‐8% decrease in number every 10 yrs.
 Mitochondria

 Make up 40% of our heart cells

 Regulates how every cell ages, divides and dies
 Control which genes are turned on or off
 Maternally inherited
 Not well protected
 Adults posses 10 million billion mitochondria, which corresponds to 10%
of our body weight.

 Easy to damage!
 Mitochondria are easily injured

 Oxidative stress (rusting)

o toxins in our environment (heavy metals, chemicals)
o Drugs (Statins‐lower coq 10 levels which impair
mitochondria function)
o Infections
o Stress(physical & emotional)
o Dysbiosis
o Poor Diet‐(High sugars, trans fats, and high
inflammatory foods)
o Chronic Diseases (DM2, Hypothyroidism,
hyperlipidemia)
Common symptoms of Mitochondrial Dysfunction

 Low energy
 Fatigue (most common symptom)
 Memory loss
 Weakness
 Cramping
 Accelerated aging
 Increased pain
 Obesity
 Drug induced Mitochondrial Toxicity

 Drugs that injure Mitochondria usually do so by inhibiting respiratory

complexes of the electron chain
 Inhibit or uncouple Oxidative Phosphorylation
 Inducing Mitochondrial stress
 Inhibiting DNA replication, transcription, or translation
 What Medications damage Mitochondria?

 Medications:
 TCA’s (Amitriptyline, Imipramine)
 Statins
 Sulfonylureas
 Oral contraceptives
 Alpha2‐adrenergic (clonidine)
 Beta –Blockers (propranolol)
 Vasodilators (hydralazine)
 Fibric Acid –(Gemfibrozil)
 Thiazide Diuretics
 Phenothiazine derivatives (Chlorpromazine)
 Analgesics: Acetaminophen, diclofenac, naproxen, ASA, Celecoxib
 SSRI’s: Citalopram, Fluoxetine
 Antibiotics: erythromycin and tetracycline
 Anti‐anxiety: Alprazolam, Diazepam, Clonazepam, Lorazepam
 Drugs that Deplete Co Q10 affect Mitochondrial function
 What damages Mitochondria?

Overeating‐causes the biggest injury to our mitochondria over time.

 Free radicals are produced by the mitochondria as it metabolizes the food
with the oxygen we breathe.
(The more food with “empty calories “you eat the more free radicals that
get produced.
 Free radicals—produced oxidation‐‐‐can damage the mitochondria‐‐
oxidize lipoproteins (LDL)‐atherosclerosis
 We protect ourselves by the amount of antioxidants in our body and our
diet (colorful fruits and veggies)
 What damages Mitochondria?

 American Diet :
 High sugars
 Flours
 Trans fats/processed foods
 Lacks antioxidants (colorful fruits and vegetables)
 Produces too many free radical’s and oxidative damage to our mitochondria
 Contributing to obesity, chronic fatigue, diabetes, heart disease, and dementia
 Chronically high blood sugar levels from HFCS, white flour, potatoes, soft drinks ..etc
cause AGE’s‐contribute to the oxidative damage to our mitochondria.
 What are AGE’s

 AGEs (Advanced Glycation End‐products) are harmful compounds that

form when excess protein and sugar bind together.
 These compounds prematurely age our bodies and have been linked to
many different serious illnesses. (CAD, DM2, Dementia, CVA, CRF, Cancer,
Arthritis…)
 AGEs are a product of a person’s lifestyle and habits. The foods we eat, the
amount of sleep we get, the stress we experience, and the level of exercise
we take part in all help determine our AGE levels.
 Smoking contributes to AGE development.
 AGE’s

 Formed inside our body when excess sugar and protein combine. (HAIC)
 They accumulate in our body damaging our mitochondria and other
tissues.
 Foods high in AGE’s: Fried foods, Sugary, processed foods, and animal
meats
 Sedentary lifestyle‐ increases AGE’s
 How you cook your food affects the amount of AGE’s
 AGE’s

 High levels of AGE’s:

o High levels of heat or overcooking
o Browning foods, barbecuing, frying, broiling, and toasting.

 Lower levels of AGE’s

 (cook with water!)

 Acidic marinades on meats can lower AGE’s by 50 %

 Foods containing phytonutrient ‐Iridoids

o Noni fruit
o Blueberries
o olive leaves
o Cranberries
o Cornelian cherries
 Oxidative metabolism

 Term we use when mitochondria are using primarily carbs as its fuel
because oxygen is consumed during the process of ATP production.
 As a by‐product the mitochondria produce ROS (reactive oxygen
species) or free radicals.
 Mitochondrial Dysfunction

 Any process that increases free radicals and oxidative stress will affect the
number and functioning of your mitochondria.
 Overeating is number1!
 Anything that causes inflammation in your body
 Poor exercise habits
 Poor sleep
 Physical or emotional stress
 Poor diet
 Environmental toxins
 Smoking
 Medications
 Mitochondria Defense

REDOX System‐helps us maintain mitochondria

 Reduction‐ neutralizes the damage from oxidation (rusting)
 Antioxidants from colorful foods and vegetables
 We need a wide variety of antioxidants to support this system‐ (not
just one)
 Not all oxidation is in our body is bad
o Wbc release hydrogen peroxide to kill viruses and bacteria.
o Adaptive changes occur in our body to oxidation which turn on protective
pathways.
(Antioxidant defenses are unregulated in conjunction with OxPhos to offset
the effects of increased ROS/free radicals.)
 After anti‐oxidants are used they become oxidants, which can
damage us, until they are neutralized in our body by one of our
master antioxidants like glutathione.
 Ketones and Mitochondria

 Ideal fuel for our body? (non‐glycating or caramelizing)

 Can starve some cancer cells
 Mitochondria function better on a ketogenic diet
 Ketogenic diet‐induces epigenic changes that increase the output of ATP
from our mitochondria via mitochondrial biogenesis.
 Improves GABA production in the brain
 May help relieve pain
 Ketogenic Diet

 Fatty acid oxidation is more efficient process than with carbohydrates

o More energy is produced with less ROS/free radicals
o Unfortunately mitochondria prefer carbs over fats if both are available.
 Healthy fat as fuel causes lower levels of free radicals than carbs as fuel.
 Ketone bodies (beta‐hydroxybutyrate and acetoacetate) produced by your
livers mitochondria when fat is the major source of food. They can fuel
your brain
 Ketones from Omega‐3 may decrease cognitive decline in old age
 Anti‐inflammatory effect
 Is there a benefit to using coconut oil or
butter as your fat?

 Carnitine palmitoyltransferase 1 (CPT1) is a major control point for the

entry of long‐chain fatty acids into the mitochondrion
 Circumvent CPT1 by consuming medium‐chain fats like coconut oil and
butter, rather than fats that contain long‐chain fatty acids.
 Medium‐chain fatty acids are metabolized differently than long‐chain
fatty acids because they can diffuse across plasma membranes without
the help of transporter proteins.(CPT1)
 If the gatekeeper CPT1 proteins are either down regulated or present in
insufficient amounts that would limit long chain fatty acids oxidation.
 It seems MCT oils have an easier time getting into the mitochondria to get
oxidized bypassing the gate keeper protein CPT1.
 Is obesity caused from Mitochondrial dysfunction?

 Growing body of research‐altered mitochondrial energy production in

skeletal muscles‐sets off the chain of metabolic events leading to obesity
 ? Younger‐ healthier mitochondrial function‐thinner‐eat Whatever you
want
 ? Older‐ lower mitochondrial function‐more sensitive to carbs‐heavier
 Obese individuals have a decreased ability to oxidize or burn free fatty
acids for use as energy in skeletal muscle.
o Defective mitochondria impair lipid oxidation causing fat storage instead of
burning it.
 Obesity

 Reasons that obese people may have difficulty burning/oxidizing fat

 Less number of mitochondria
 Smaller mitochondria
 Structural problems‐ ER unwinding
 Poor functioning (reduced oxidative capacity)
 Acyl‐carnitine accumulation and ceramide formation

 Mitochondrial dysfunction‐plausible explanation for some forms of

obesity
 Poor lipid oxidation leads to storage of fat
 Weight loss by itself does not improve fatty acid oxidation in mitochondria
o High carb diet after dieting‐regain all of your weight
 Insulin resistance –leads to obesity

 A condition in which cells fail to respond to the normal actions of the

hormone insulin.
 Can be caused by intracellular fat accumulation in muscles and liver.
 In lean individuals, the inability of the mitochondria to burn fat in muscle
because of dysfunction will cause insulin resistance.
 Rats bred for low mitochondrial activity that were fed high fat diets gained
more weight, added more fat, and became more insulin resistant
 Muscle Biopsy

 Has been one of the best ways to determine mitochondrial disease and
dysfunction
 Using Genetic microarray chips and advanced microscopes‐allow researchers to identify
molecules that support healthy mitochondria
 Muscle biopsies of obese individuals
 More mitochondrial dysfunction (impaired oxidation phosphorylation) and reduced
mitochondrial content
 Accumulation of fat in muscle.
 The more abundant mitochondria you have the more efficient your body works

 Most obese patients have mitochondrial dysfunction.

 Obesity

 For fat loss to occur, fat must be mobilized from fat stores and sent to
mitochondria to be used in the production of ATP.
 Increasing mitochondrial function and density will help you burn more fat
efficiently.
 Difference brown fat and white fat

 Brown fat‐ higher concentration of mitochondria‐

more blood supply
 White fat‐packed with lipids‐less metabolically
active‐ less blood supply
Not all Mitochondrial dysfunction causes poor health:
 Sometimes mutations in electron transport chain that cause
mitochondrial dysfunction can paradoxically lead to to improved
health.
 Mice‐ knockout of transcriptional factor A (TFKO)
 Exhibit mitochondrial dysfunction with increased energy
expenditure
 Protected from age and diet –induced obesity, insulin
resistance and fatty liver despite increase in food intake.
 Despite reduction in transcription factor mitochondria‐ no
difference in the number of mitochondria seen in brown vs.
white fat (control vs. KO group)
 TFKO –decreased mitochondrial DNA in electron transport
chain
o Causes altered levels of proteins in electron transport chain
o Decreased complex1 activity
o Greater oxygen consumption
o Increased uncoupling of respiration
AGING, Vol 4, No 12 , pp 859-860
Not all Mitochondrial dysfunction
causes poor health:
o As a result increase in oxidative capacity increased
o In normal mice‐no increase of of oxidative stress
damage
o Upon high fat diet‐build up of acyl carnitines, oxidative
stress/overload ROS‐the mice remain lean with
normal insulin sensitivity.
o Increased adiponectin mRNA in white fat‐ decreasing
fat mass
o 50% reduction in adiponectin levels (impairment
complex1)
AGING, Vol 4, No 12 , pp 859-860
 How Can Mitochondrial biogenesis help
with weight loss?

 Increasing the number and function of mitochondria may be the way to

reverse obesity, through the activation of PGC‐1a which stimulates
mitochondrial biogenesis.

 What is PGC‐1a?
 PGC‐1alpha (peroxisome proliferator‐activated
receptor‐gamma coactivator‐1 alpha)

 Master regulator of mitochondrial biogenesis. “EXERCISE Molecule”

 It increases expression of NRF‐1 (nuclear respiratory factor‐1) and mtTFA
( mitochondrial transcription factor a) which turns on the production of
nuclear and mitochondrial genes.

 Functions as a transcription factor‐protein that binds to your DNA to

regulate new protein synthesis‐Your Mitochondria
 Increased PGC‐1alpha‐ improves exercise performance
 PGC‐1alpha
 Increased PGC‐1alpha‐ improves exercise performance

o Genetically altered mice that produced higher than normal amounts of PGC‐1a
in there skeletal muscle had less fatigue in their slow twitch muscles, greater
running ability, improved endurance and recovery, and much greater
Mitochondrial content.
o Rat’s exposed to prolonged cold temperature up‐regulated PGC‐1a as a response
to increased intracellular calcium through brown adipose activation.
 Ultimate goal for all of our patients‐Increase
mitochondrial biogenesis and function!

 Decreases ROS/Oxidative stress

 Improves Metabolic function
 Increases Energy levels
 Increases exercise performance
 Decreases Body Fat & increases Lean muscle
 Decrease Chronic illnesses of ageing
 How to stimulate new Mitochondria?
Strategies to reinvigorate Mitochondria

1. Regular exercise
2. Transient caloric restriction
3. Low carb diets
4. Supplement with nutrients

All of these pathways lead to stimulate PGC 1a

 Strategies to reinvigorate Mitochondria

Low Carb Caloric Nutritional

Diet Exercise
Restriction interventions

Increased
PGC1a

Increased mitochondrial
biogenesis
Decreased body fat
Increased lean muscle mass
Exercise and Mitochondrial Biogenesis

 Mitochondria capacity can decline with age, disease and

weight gain
 Mitochondrial number is not fixed.
 Mitochondrial biogenesis is a complex system.
 The best way to produce mitochondria is exercise!
 Sedentary lifestyle‐ increases DM, CAD, and Dementia.
 Exercise has many benefits not just reducing fat.
 Lowers risks for DM, CAD, neurodegeneration and
cancer whether or not you our overweight or not.
 Exercises increases mitochondrial activity in older
patients, (resistance, aerobic and HIIT)
 Cellular triggers or second messengers

 Occur when going from rest to high level of activity

 Second messenger signaling molecules pass the message that the muscle
is now active and very specific metabolic and mechanical challenges are
needed.
 Muscle contraction‐releases ca++ and other products—act as second
messengers to activate the system.
o CaMK (Calcium/calmodulin‐dependant protein kinase)
o Stimulates the uptake of glucose into the cell to support the increased metabolic
need.
o Increases PGC‐1a
 Cellular triggers or second messengers

 The signals generated at low intensity aerobic exercise differ from high
intensity resistance exercise.
o This explains the long term adaptations that occur with different types of
training
o Aerobic activity‐ increases mitochondrial functioning better than resistance
training
o Resistance training increases the contractile machinery better than aerobic
training (sprinter vs. marathon runner)
 5AMPK‐(Adenosine monophosphate activating protein kinase)

 Master switch‐ turning on cellular metabolism

 Turns on and off quickly
 Senses low levels of ATP
 Stimulates glucose uptake into the cell‐glycolysis
 Senses changes in the ratio of creatine to phosphocreatine
o Phosphocreatine is used at the onset of exercise to produce ATP
o Its converted to creatine
 Activates fatty acid and triglyceride oxidation in muscle and liver cells providing
a better source of energy for the cellular production of ATP compared to
carbohydrate metabolism.
 It has been a molecular target for increasing energy expenditure, improving
insulin sensitivity, and reducing appetite.
 Contributes to the long term adaptation of muscle by Activating PGC‐1a and
Mitochondrial Biogenesis.
 NO (Nitrous Oxide)

 Exercise induced second messenger

 Produced from L‐arginine and oxygen by Nitric oxide synthase
 Increases cGMP
 Increased by exercising
 Contributes to long term adaptations of our body
 Relaxes smooth muscles in our arteries to deliver more fuel to our
contracting muscles
 Stimulates the uptake of glucose into our muscles
 Potent stimulator of PGC‐1a and Mitochondrial Biogenesis
 Increase NO

Exercise Increase CaMK

Increase AMPK

Exercise increases these 3 secondary messengers allowing

cellular adaptation to increase work load
These 3 second messengers turn on PGC 1‐alpha
resulting in mitochondrial biogenesis

CaMK

NO AMPK

PGC1a
Caloric Restriction‐Is there a benefit?

 135 study Professor Clive McCay from Cornell

o rats fed a diet 30‐40% fewer calories lived 33% longer
than there counterpart rats who could eat as much as
they wanted
 Dietary restriction in other species has produced
similar results
 Some early studies in humans are suggesting
improved biomarkers of health
 Caloric Restriction

 The benefits are due to caloric restriction and not from a dietary
component
o Studies have disproved that there was a single macronutrient,
multivitamin, or antioxidant (Vitamin C &E) that was the cause of the
benefits seen from calorie restriction.
 Caloric Restriction

o Theories:
o Caloric restriction slows cell division (delay in cancer with rodents)
o Caloric restriction slows the formation of AGE’s which causes less
mitochondrial damage from ROS (free radicals)
o Stimulates Sirt1 gene
 Sirtuins

 The sirtuin family of genes works by protecting and improving the health
and function of your mitochondria

 They are positively influenced by a diet that is non‐glycating, i.e. a low

carb diet as opposed to a high carb diet which induces mitochondrial
dysfunction and formation of reactive oxygen species.
 The Gene SIRT1 was discovered during the search for genes and proteins
during caloric restriction.
 SIRT1

 SIRT1 (Silent information regulator of transcription

o Its protein is increased by caloric restriction and exercise

o In mice with overexpressed SIRT1 they live longer and have healthier
metabolisms ( make more ATP) and are more resistant to disease.

o Has been called the “Fountain of youth Gene”

o Activates PGC‐1a to produce more mitochondria

 Increases Increase
Caloric
SIRT1 Increases PGC1-a Mitochondrial
Restriction
Biogenesis
Nutritional interventions that allow us to stimulate
the pathways of mitochondrial biogenesis

o French Paradox‐French consume a higher amount of

saturated fat but have a lower risk for CV disease. There
are theories that the red wine that they drink protects
them.

o What’s in Red wine that could protect us?

o These studies allowed us to understand the pathways and

some of the nutritional agents that could mimic the
beneficial effect of caloric restriction.
 Resveratrol

o a polyphenolic compound found in grapes and peanuts (stilbenol)

o red wine contains the highest amount (0.1‐14.3 mg/liter)
o poor oral bioavailability, rapid ½ life‐10 min
o methylated resveratrol‐has a longer half life and 5‐8 x better absorption
o In animal studies:
o Anti‐cancer activity
o Cardiovascular protection
o Antioxidant
o Protective effect for glutathione
o Anti‐inflammatory effect
o Anti‐viral effects
o Protective for neurodegenerative diseases
o Improve lifespan and delay age related deterioration
 Resveratrol

 Activates all 3 messengers: SIRT1, AMPK, NO production

 Protected mice from diet induced obesity and insulin
resistance
 It mimics the effects of caloric restriction and exercise
 Resveratrol activates SIRT1 and PCG-1a to stimulate
mitochondrial biogenesis
 Quercetin

 Polyphenolic antioxidants found in capers, onions, and apples

 Extends the duration of resveratrol by inhibiting its breakdown in the liver
 Activates SIRT1 (not as powerful as resveratrol)
 Anti‐inflammatory effects
 Shuts down fat storage
 Increase muscle and brain mitochondrial production
 May improve Vo2 max
 Rutin

 Rutin Increases Muscle Mitochondrial Biogenesis with AMPK Activation in

High‐Fat Diet‐Induced Obese Rats
 Rutin (rutoside, quercetin‐3‐O‐rutinoside and sophorin) is a flavonol
glycoside composed of quercetin and disaccharide rutinose and is
present in many plants, including buckwheat

Nutrients 2015, 7, 8152-8169; doi:10.3390/nu7095385

 L-Arginine

 Amino acid derivative

 Improved effectiveness with addition of alpha ketoglutaric acid (AKG)
 Enhances calorie burning by increasing mitochondrial function
 Precursor to NO (nitric oxide)
 Dilates blood vessels‐improves blood pressure and circulation
 Stimulates mitochondria production through activation of PGC1a
 Studies reveal:
o improves strength and speed
o improves fat burning and muscle gain
o enhances exercise performance and duration
 R-Alpha Lipoic Acid

 Short half life (30 min)

 Reduces plasma fructosamine
 Decreases appetite‐ by decreasing AMPK in hypothalamus (negative
feedback)
 Increase Vitamin C, E and Coq 10’s function in your body
 Improves brain and nerve function
 Improves liver/kidney function
 Prevent migraines
 Treat or prevent Heart disease
 R-Alpha Lipoic Acid

 Increases AMPK in skeletal muscle

 Increases fat burning (reduces the triglyceride levels in the muscles)
 Increases mitochondrial energy output
 Stimulates mitochondrial production
 Studies‐Heals tendon injuries
 ‐Treat Diabetic neuropathy
 ‐ improves weight loss
 ‐ Improves PCOD
 ‐ improves glucose control in DM2
 Nicotinamide Riboside

o Helps to regulate NAD levels improving SIRT 1, and SIRT 3 function

o Increases PGC1a to stimulate mitochondrial biogenesis and energy
production.
o Its more efficient in recycling NAD for proper SIRT activation (avoids the
rate limiting step)
o In mice, it reduced body weight in high‐fat mice, improved lean body
mass, improved insulin sensitivity, and reduced total cholesterol.
 Acetyl-L Carnitine

 Reduce physical and mental fatigue in elderly

 Improves exercise capacity in patients with heart failure
 Improve in physical performance and fatigue recovery
 Activates PGC1a

 Dr. Bruce Ames‐University of Calif @Berkley

 Older Rats given ALA & Acetyl‐L carnitine improved their endurance and
activity
 Acetyl-L Carnitine

 A recent study by Juvenon founder, Dr. Tory Hagen showed (in rats) that
supplementation with acetyl‐L‐carnitine (ALCAR) can reverse the age‐
related decline in fatty acid transport into mitochondria. This was most
likely because the ALCAR stimulated PGC‐1alpha and mitochondrial
renewal. Acetyl‐L‐carnitine supplementation also reversed the age‐related
decline in carnitine palmitoyltransferase 1 (CPT1) activity in interfibrillar
mitochondria without changing the L‐carnitine content in the rat heart.
CPT1 is important because it helps regulate the oxidation of fat into
energy in the mitochondria
 Coenzyme Q10

o Participates in the production of adenosine triphosphate (ATP) as part

of the electron transport chain
o Protects the mitochondria against free‐radical damage.
o Reduced by Statins and many drugs.
 PQQ (pyrroloquinoline quinone)

o 2010 research at UC Davis‐protection of mouse liver from from oxidative stress

and promoted new mitochondria
o stimulates PGC1a via c‐AMP
o protects against DJ‐1 oxidation (neuro‐protective role)
 PGC-1α: Improved Glucose Sensitivity & Mitochondrial Function
= Weight Loss, Increased Endurance
 Peroxisome proliferator-activated receptor gamma coactivator-1-alpha (PGC-
1α) induces expression of genes in skeletal muscle for gluconeogenesis,
mitochondrial fatty acid oxidation, and mitochondrial biogenesis. Treatment
with resveratrol that results in Sirt1 deacetylation of PGC-1α rapidly improves
insulin sensitivity and glucose tolerance in obese mice; a longer treatment
course lowers body weight, induces mitochondrial biogenesis, eliminates
ectopic fat deposits, and increases endurance.
PQQ mouse
 Green Tea extract
(Camellia sinesis)

EGCG ‐‐ a compound found in most green Tea

 Limits the fat that we absorb
 Enhances the ability to burn fat
 Antioxidant for many pathways in our bodies and protects our DNA from
damage
 Effects gene signaling in our bodies
 Selectively improves the function of intestinal bacteria
 Has been used to treat elevated Enox 2 levels in tumors
 Increases PGC‐1a, Sirtuin 3
 SIRT 1 Stimulators

Polyphenols:
 Resveratrol-13 fold increase
 Piceatanol-(metabolite of resveratrol)-7.9 fold increase
 Curcumin-(Curry spice)
 Fisetin- (found in strawberries)- 6.6 fold increase
 Quercetin- found in capers and apples)-4.6 fold increase
 EGCG (Green Tea)
 Butein (Jap Laquer tree)-8.5 fold increase

Howitz and Sinclair

 Resveratrol
Quercetin
Green tea
L-arginine PQQ R-Alpha Lipoic
Alpha Ketoglutarate acetyl-l-carnitine Acid
Amino Acids Rutin
Exercise

Increased Increased
Increased NO
SIRTUINS AMPK

Increased
PGC1a

Increased mitochondrial biogenesis

Decreased body fat
Increased lean muscle mass
 Conclusions:

 Target mitochondrial Biogenesis through increasing PGC1a

This results in:

 Decreases ROS/Oxidative stress
 Improves Metabolic function
 Increases Energy levels
 Increases exercise performance
 Decreases Body Fat & increases Lean muscle
 Decrease Chronic illnesses of ageing
 Conclusion

 Focus on restoring Mitochondrial function in your obese population for

long term success

 Target mitochondrial Biogenesis through increasing PGC1a by:

o Exercise #1
o Caloric restriction ( low Carb diets)
o Nutraceutical focused on increasing: (NO, SIRT1, AMPK)
 Once you restore your mitochondrial function

 Continue to decrease carbs in the diet

 Regular exercise
 Meal
o Low glycemic carbs (colorful vegetables and small portions of lower glycemic
fruits)
o Moderate Organic lean proteins
o High in Healthy fats‐Omega ‐3, omega‐9 , MCT’s Coconut oil and Butter‐(keeps
the mitochondria burning fat)
o Avoid high glycemic carbohydrates as snacks.
Thank You!

Anthony L. Capasso, MD
Chief Medical Officer
Thin Centers MD
Ponte Verdra, Florida