Martha Stark MD – 26 Jun 2009 – The Overwhelmed Heart.pptx

M
Martha Stark MDFaculty, Harvard Medical School / Integrative Psychiatrist and Holistic Psychoanalyst / Originator and Developer, The Psychodynamic Synergy Paradigm: A C.A.R.E. Approach to Deep Healing em Harvard Medical School
MURMUR OF THE HEART:
THE STORY IT TELLS WHEN WE LISTEN
MARTHA STARK, M.D.
marthastarkmd@hms.harvard.edu
Friday, June 26, 2009
CORONARY ARTERY DISEASE
THE “SILENT” KILLER
STEPHEN SINATRA – ”… 90% OF CORONARY DISEASE
IS ASYMPTOMATIC – A SILENT PROCESS ERODING THE ARTERIES.
IN HALF THOSE CASES, SUDDEN DEATH IS THE VERY FIRST SYMPTOM.”
S Sinatra. Reverse Heart Disease Now. Hoboken, NJ: John Wiley, 2007.
INSIDIOUS DEVELOPMENT OF CORONARY ARTERY DISEASE
OFTEN NO OBVIOUS INDICATIONS THAT OUR CORONARY ARTERIES
HAVE BECOME COMPROMISED,
WHICH COMPROMISES THE HEART,
WHICH COMPROMISES THE VASCULAR SYSTEM,
WHICH COMPROMISES THE CELLS
IF WE PAY CLOSE ENOUGH ATTENTION TO THE VARIOUS CLUES
THAT OUR TELL-TALE HEARTS ARE OFFERING US,
THEN WE MAY BE ABLE TO AVERT A POTENTIAL CARDIAC CRISIS
BY TAKING ACTION
SYMPTOMS AND BLOOD WORK
CHEST PAIN, SHORTNESS OF BREATH, FATIGUE, ARRHYTHMIAS
CoQ10 ($135) – ATP PRODUCTION
hs-CRP ($33) – INFLAMMATION
FERRITIN ($36) – OXIDATION OF LDL, PLAQUE, INFLAMMATION
RBC MAGNESIUM ($52) – ATP PRODUCTION
FIBRINOGEN ($25) – BLOOD VISCOSITY
HOMOCYSTEINE ($82) – PLAQUE, BLOOD CLOTS
LIPOPROTEIN(a) ($46) – PLAQUE
TOTAL LIPID PROFILE (INCLUDING OXIDIZED LDL)
AA / EPA RATIO – RELATIONSHIP BETWEEN PRO - INFLAMMATORY AA
AND CARDIOPROTECTIVE ANTI - INFLAMMATORY EPA
FASTING BLOOD SUGAR / FASTING INSULIN / HEMOGLOBIN A1c –
INSULIN RESISTANCE
SEX HORMONES
THYROID PROFILE INCLUDING TSH (AND THYROID ANTIBODIES)
BLOODS SHOULD BE WITHIN THE OPTIMAL RANGE
EXCESS FAT
65 – 70% OF PEOPLE IN US ARE EITHER OBESE OR OVERWEIGHT
National Health and Nutrition Examination Survey (NHANES) 2001 – 2004.
RISK FACTOR – EXPANDED GIRTH
WAIST CIRCUMFERENCE OF >40” IN MEN, >35” IN WOMEN
“APPLES” TEND TO ACCUMULATE FAT AROUND THE WAIST
AND ARE MORE AT RISK FOR DEVELOPING ATHEROSCLEROSIS
THAN ARE PEOPLE WHO ARE “PEARS”
ABDOMINAL FAT STIMULATES THE PRODUCTION OF
PRO – INFLAMMATORY SUBSTANCES (e.g., C – REACTIVE PROTEIN)
AND PUTS EXCESS PRESSURE ON THE INTERNAL ORGANS,
MOST IMPORTANTLY THE HEART
OBESITY – ASSOCIATED WITH INCREASE IN TOTAL BLOOD VESSEL
LENGTH IN ORDER TO REACH THE ADIPOSE TISSUE
THIS INCREASED LENGTH INCREASES THE PERIPHERAL RESISTANCE,
WHICH INCREASES THE BLOOD PRESSURE REQUIRED
TO MAINTAIN BLOOD FLOW
RISK FACTORS /
ENVIRONMENTAL STRESSORS
IMPACT OF CARDIAC RISK FACTORS / STRESSORS –
SYNERGISTIC, NOT JUST ADDITIVE
SOME WE ARE BORN WITH, SOME WE ACQUIRE OVER TIME
OVER SOME WE HAVE LITTLE OR NO CONTROL
OVER MANY WE HAVE COMPLETE CONTROL
CRUCIAL THAT WE ADDRESS ALL RISK FACTORS / STRESSORS
BY LIGHTENING THE LOAD
(TO CORRECT FOR TOXICITIES)
AND REPLENISHING THE BODY RESERVES
(TO CORRECT FOR DEFICIENCIES)
TO RESTORE THE UNDERLYING RESILIENCE AND ADAPTABILITY
OF A HEART UNDER SIEGE
RESTORE RESILIENCE
LIGHTEN THE LOAD – BY WAY OF
SAUNAS, HEAVY METAL CHELATION,
SWEATING, MASSAGE, COLON CLEANSES,
BLOOD DONATION
REPLENISH THE RESERVES – BY WAY OF
A WHOLE – FOODS, ORGANIC DIET
RICH IN NATURAL FIBER
SUPPLEMENTED WITH THE FOLLOWING –
FISH OIL, NATTOKINASE (NATURE’S CLOT BUSTER),
CoQ10, D – RIBOSE, L – CARNITINE, MAGNESIUM,
L – ARGININE, VITAMIN C, VITAMIN E, VITAMIN D3,
NIACITOL (A COMBINATION OF NIACIN AND INOSITOL),
VITAMIN K, RED YEAST RICE, AGED GARLIC EXTRACT,
LYCOPENES, BIOFLAVONOIDS, PANTETHINE, POLICOSANOL,
PHOSPHATIDYLCHOLINE, GREEN TEA
THE ADAPTABLE HEART
WHEN THE CUMULATIVE IMPACT OF STRESS AND STRAIN
GIVES RISE TO ISCHEMIA AND CARDIAC PAIN
LIGHTEN THE LOAD, REPLENISH THE RESERVES,
AND PROVIDE THE SUPPORT THE POOR HEART DESERVES
IN ORDER THAT FLOW TO RESTORE, GOOD HEALTH TO REGAIN.
Martha Stark (2009)
HEART MUSCLE –
FIRST AND FOREMOST A PUMP
HEART – A PUMP; BLOOD VESSELS – HOSES
WHEN CHALLENGED, THEY WORK HARDER
IN AN EFFORT TO RESTORE HOMEOSTATIC BALANCE,
THEY RESPOND TO THE CHALLENGE BY ADAPTING TO IT
BUT WHEN CHALLENGED REPEATEDLY,
THE HEART AND BLOOD VESSELS WILL WEAR OUT
IN THE SHORT – TERM, THE STRESS RESPONSE IS VITAL
IT CAN SAVE OUR LIVES
BUT, IN THE LONG – TERM, IT CAN MAKE US VERY SICK
STEPHEN SINATRA – STRESS IS NOT WHAT HAPPENS TO US
BUT HOW WE REACT TO WHAT HAPPENS
NARROW MARGIN OF SAFETY
AND HIGH STAKES
THE HEART IS PARTICULARLY VULNERABLE TO STRESS
BECAUSE THE MARGIN OF SAFETY
BETWEEN THE DOSE OF STRESS THAT THE HEART CAN MANAGE
AND THE DOSE OF STRESS THAT IT CANNOT
IS VERY NARROW
AND A HEART DAMAGED BY STRESS
CAN LEAD TO IMMEDIATE DEATH
WITH RESPECT TO A SYSTEM AS VITAL AND VULNERABLE
AS THE CARDIOVASCULAR SYSTEM,
ENVIRONMENTAL STRESSORS THAT CANNOT BE ADAPTED TO
WILL BE THE OCCASION FOR CARDIAC EVENTS
THAT COULD WELL BE FATAL
CRUCIAL THEREFORE TO SUPPORT THE HEART
BY LIGHTENING ITS LOAD AND REPLENISHING ITS RESERVES
OXYGEN
UNDER RESTING CONDITIONS, MOST TISSUES IN THE BODY
EXTRACT ONLY ABOUT 25% OF THE OXYGEN AVAILABLE
BUT CAN ADAPT TO INCREASED METABOLIC DEMANDS
BY IMMEDIATELY REMOVING A GREATER PERCENTAGE OF OXYGEN
BY CONTRAST, THE HEART, EVEN UNDER RESTING CONDITIONS,
ALREADY REMOVES UP TO 65% OF THE OXYGEN AVAILABLE
FURTHERMORE, THE HEART HAS LITTLE ABILITY TO SUPPORT ITS
ENERGY NEEDS BY MEANS OF ANAEROBIC METABOLISM
AND MUST RELY HEAVILY ON ITS OXYGEN SUPPLY
THEREFORE, THE PRIMARY MEANS BY WHICH MORE OXYGEN
CAN BE MADE AVAILABLE TO THE HEART MUSCLE
IS BY INCREASING CORONARY BLOOD FLOW
BUT THE HEART CAN TOLERATE WIDE VARIATIONS
IN ITS NUTRIENT SUPPLY (FATTY ACIDS, GLUCOSE, LACTATE)
SO THE PRIMARY DANGER OF INSUFFICIENT CORONARY BLOOD FLOW
IS NOT FUEL SHORTAGE BUT OXYGEN DEFICIENCY
SYSTEM OF BIFURCATION
LARGE BLOOD VESSELS BRANCH INTO SMALLER VESSELS,
THEN INTO EVEN SMALLER ONES, AND SO ON,
DOWN TO TINY BEDS OF THOUSANDS OF CAPILLARIES
NO CELL IN THE BODY IS MORE THAN FIVE CELLS AWAY FROM
A BLOOD VESSEL – THOUGH THE CIRCULATORY SYSTEM ITSELF
OCCUPIES ONLY 3% OF THE BODY MASS
THE POINTS OF BIFURCATION ARE
PARTICULARLY VULNERABLE TO INJURY
WITH THE CHRONIC INCREASE IN BLOOD PRESSURE
THAT ACCOMPANIES CHRONIC STRESS
AND INCREASED SYMPATHETIC ACTIVITY,
DAMAGE BEGINS TO OCCUR AT THESE BRANCH POINTS –
AND THE SMOOTH INNER LINING OF THE VESSELS
BEGINS TO BREAK DOWN
CHRONIC STRESS CAUSES PLAQUE
ONCE THIS LAYER OF CELLS IS DAMAGED,
THE FATTY ACIDS AND GLUCOSE THAT HAVE BEEN MOBILIZED
INTO THE BLOODSTREAM BY THE STRESS RESPONSE
BEGIN TO WORK THEIR WAY UNDERNEATH THIS LAYER,
WHERE THEY GET STUCK, CAUSING A THICKENING OF THE LINING
ALSO, DURING STRESS, THE BLOOD BECOMES MORE VISCOUS
BECAUSE OF THE CLUMPING TOGETHER OF PLATELETS
WHERE THERE ARE TEARS IN THE LINING OF THE BLOOD VESSELS,
THESE CLUMPS OF PLATLETS WILL AGGREGATE,
COMPOUNDING THE PROBLEM
MOREOVER, FOAM CELLS WILL ALSO BEGIN TO GATHER
OVER TIME, THE VESSELS WILL BECOME
PARTIALLY OR TOTALLY BLOCKED,
MAKING IT MORE AND MORE DIFFICULT FOR THE BLOOD TO FLOW
ATHEROSCLEROSIS AND HYPERTENSION –
RISK FACTORS BUT ALSO ADAPTIVE
HARDENING OF THE ARTERIES AND HYPERTENSION,
ALTHOUGH ASSOCIATED WITH SIGNIFICANTLY INCREASED RISK
OF HEART DISEASE, ARE ALSO ADAPTIVE MECHANISMS
TWO HOSES – BOTH TEN FEET TOO SHORT TO REACH THE FIRE
ONE HOSE – A DIAMETER OF THREE FEET
WITH SOFT, DISTENSIBLE WALLS
THE OTHER HOSE – A DIAMETER OF ONE INCH
WITH HARD, RIGID WALLS
HARDENED ARTERIES MAKE FOR INCREASED BLOOD PRESSURE,
NECESSARY TO GET THE BLOOD TO WHERE IT NEEDS TO GO
BUT BOTH ARE OBVIOUSLY ADDITIONAL STRESSORS FOR THE HEART,
WHICH WILL HAVE TO WORK HARDER TO GENERATE
THE FORCE NEEDED TO OFFSET THE RESISTANCE
OFFERED BY THE HARDENED ARTERIAL WALLS
ATHEROSCLEROSIS AND HYPERTENSION
CAN THEMSELVES PROMOTE
ADAPTIVE COLLATERALIZATION
HARDENED ARTERIES AND ELEVATED BLOOD PRESSURE,
ALTHOUGH MAJOR RISK FACTORS,
ARE THEMSELVES TRIGGERS FOR
THE FORMATION OF COLLATERAL BLOOD VESSELS
NATURE’S INGENIOUS WAY OF CREATING
ALTERNATE ROUTES FOR OBSTRUCTED BLOOD FLOW
COLLATERALIZATION,
PARTICULARLY OF CORONARY ARTERIES,
IS A WONDROUSLY ADAPTIVE MECHANISM
EMPLOYED BY THE BODY
TO RESTORE HOMEOSTATIC BALANCE
IMPACT OF PSYCHOLOGICAL STRESS
JAY KAPLAN AT BOWMAN GREY MEDICAL SCHOOL
STUDIED THE RESPONSE OF MONKEYS
AT THE BOTTOM OF THE TOTEM POLE
WHEN IT CAME TO A SOCIAL DOMINANCE HIERARCHY
MONKEYS AT THE BOTTOM OF THE HEAP
ENDED UP WITH THE MOST SERIOUS ATHEROSCLEROSIS
IN A VARIATION ON THIS EXPERIMENT,
KAPLAN KEPT THE DOMINANCE HIERARCHY UNSTABLE
BY SHIFTING THE MONKEYS INTO NEW GROUPS EVERY MONTH,
SO THAT ALL THE ANIMALS WERE PERPETUALLY TENSE
AS THEY JOCKEYED FOR A GOOD POSITION ON THE TOTEM POLE
THE MONKEYS PRECARIOUSLY HOLDING ON TO THEIR PLACES
AT THE TOP OF THE SHIFTING DOMINANCE HIERARCHY
ENDED UP WITH THE MOST SERIOUS ATHEROSCLEROSIS
J Kaplan & S Manuck. Status, Stress, and Atherosclerosis.
Ann NY Acad Sci 1999;896:145-61.
DEPRESSION AS RISK FACTOR
“ALTHOUGH DEPRESSION AND HEART DISEASE
THEY CAN AND DO OCCUR SEPARATELY, RESEARCH SHOWS
THAT THE TWO CONDITIONS ARE OFTEN CONNECTED.”
DEPRESSION CAN CAUSE ABNORMAL HEART RHYTHMS,
INCRESED BLOOD PRESSURE, MORE VISCOUS BLOOD,
ELEVATED CHOLESTEROL LEVELS, ELEVATED INSULIN LEVELS,
AND ELEVATED LEVELS OF STRESS HORMONES
ALL OF WHICH INCREASE THE STRESS ON THE HEART
Mayo Clinic Women’s HealthSource – Feb 13, 2006.
Making Connections: Depression and Heart Disease.
POSTMENOPAUSAL WOMEN WITH SYMPTOMS OF DEPRESSION
AND NO HISTORY OF HEART DISEASE
HAD A 50% GREATER RISK OF DEVELOPING HEART DISEASE
THAN DID WOMEN WITHOUT DEPRESSION
S Edelstein & J Sharlin. Life Cycle Nutrition: An Evidence-Based Approach.
New York, NY: Jones & Bartlett Publishers, 2008.
THE ADAPTABILITY OF THE HEART
THE HEART IS BEING CONTINUOUSLY STRESSED
BY ALL MANNER OF STRESSORS
(PSYCHOLOGICAL, PHYSIOLOGICAL, ENERGETIC)
WHAT MATTERS WILL BE THE CUMULATIVE IMPACT
OF ALL THESE STRESSORS –
SYNERGISTIC, NOT JUST ADDITIVE
BUT WHAT REALLY MATTERS WILL BE
THE HEART’S ABILITY TO ADAPT TO THAT IMPACT
IF THE UNDERLYING ADAPTABILITY OF THE HEART
IS SUCH THAT IT CAN TAKE THE IMPACT IN ITS STRIDE,
BY MAKING THE APPROPRIATE ADJUSTMENTS,
THEN ALL WILL BE WELL
BUT IF THE HEART HAS ALREADY BEEN DAMAGED,
THEN THE HEART MAY BE UNABLE TO MANAGE THE STRESS
THE OVERWHELMED HEART
WHEN THE CUMULATIVE IMPACT OF STRESS AND STRAIN
GIVES RISE TO ISCHEMIA AND CARDIAC PAIN
IF WE LISTEN NOT TO THE MURMUR OF OUR HEART
AND PRETEND THAT IN OUR FATE WE PLAY NO PART
THEN OUR LIFE WE WILL NOT RETAIN.
Martha Stark (2009)
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Martha Stark MD – 26 Jun 2009 – The Overwhelmed Heart.pptx

  • 1. MURMUR OF THE HEART: THE STORY IT TELLS WHEN WE LISTEN MARTHA STARK, M.D. marthastarkmd@hms.harvard.edu Friday, June 26, 2009
  • 2. CORONARY ARTERY DISEASE THE “SILENT” KILLER STEPHEN SINATRA – ”… 90% OF CORONARY DISEASE IS ASYMPTOMATIC – A SILENT PROCESS ERODING THE ARTERIES. IN HALF THOSE CASES, SUDDEN DEATH IS THE VERY FIRST SYMPTOM.” S Sinatra. Reverse Heart Disease Now. Hoboken, NJ: John Wiley, 2007. INSIDIOUS DEVELOPMENT OF CORONARY ARTERY DISEASE OFTEN NO OBVIOUS INDICATIONS THAT OUR CORONARY ARTERIES HAVE BECOME COMPROMISED, WHICH COMPROMISES THE HEART, WHICH COMPROMISES THE VASCULAR SYSTEM, WHICH COMPROMISES THE CELLS IF WE PAY CLOSE ENOUGH ATTENTION TO THE VARIOUS CLUES THAT OUR TELL-TALE HEARTS ARE OFFERING US, THEN WE MAY BE ABLE TO AVERT A POTENTIAL CARDIAC CRISIS BY TAKING ACTION
  • 3. SYMPTOMS AND BLOOD WORK CHEST PAIN, SHORTNESS OF BREATH, FATIGUE, ARRHYTHMIAS CoQ10 ($135) – ATP PRODUCTION hs-CRP ($33) – INFLAMMATION FERRITIN ($36) – OXIDATION OF LDL, PLAQUE, INFLAMMATION RBC MAGNESIUM ($52) – ATP PRODUCTION FIBRINOGEN ($25) – BLOOD VISCOSITY HOMOCYSTEINE ($82) – PLAQUE, BLOOD CLOTS LIPOPROTEIN(a) ($46) – PLAQUE TOTAL LIPID PROFILE (INCLUDING OXIDIZED LDL) AA / EPA RATIO – RELATIONSHIP BETWEEN PRO - INFLAMMATORY AA AND CARDIOPROTECTIVE ANTI - INFLAMMATORY EPA FASTING BLOOD SUGAR / FASTING INSULIN / HEMOGLOBIN A1c – INSULIN RESISTANCE SEX HORMONES THYROID PROFILE INCLUDING TSH (AND THYROID ANTIBODIES) BLOODS SHOULD BE WITHIN THE OPTIMAL RANGE
  • 4. EXCESS FAT 65 – 70% OF PEOPLE IN US ARE EITHER OBESE OR OVERWEIGHT National Health and Nutrition Examination Survey (NHANES) 2001 – 2004. RISK FACTOR – EXPANDED GIRTH WAIST CIRCUMFERENCE OF >40” IN MEN, >35” IN WOMEN “APPLES” TEND TO ACCUMULATE FAT AROUND THE WAIST AND ARE MORE AT RISK FOR DEVELOPING ATHEROSCLEROSIS THAN ARE PEOPLE WHO ARE “PEARS” ABDOMINAL FAT STIMULATES THE PRODUCTION OF PRO – INFLAMMATORY SUBSTANCES (e.g., C – REACTIVE PROTEIN) AND PUTS EXCESS PRESSURE ON THE INTERNAL ORGANS, MOST IMPORTANTLY THE HEART OBESITY – ASSOCIATED WITH INCREASE IN TOTAL BLOOD VESSEL LENGTH IN ORDER TO REACH THE ADIPOSE TISSUE THIS INCREASED LENGTH INCREASES THE PERIPHERAL RESISTANCE, WHICH INCREASES THE BLOOD PRESSURE REQUIRED TO MAINTAIN BLOOD FLOW
  • 5. RISK FACTORS / ENVIRONMENTAL STRESSORS IMPACT OF CARDIAC RISK FACTORS / STRESSORS – SYNERGISTIC, NOT JUST ADDITIVE SOME WE ARE BORN WITH, SOME WE ACQUIRE OVER TIME OVER SOME WE HAVE LITTLE OR NO CONTROL OVER MANY WE HAVE COMPLETE CONTROL CRUCIAL THAT WE ADDRESS ALL RISK FACTORS / STRESSORS BY LIGHTENING THE LOAD (TO CORRECT FOR TOXICITIES) AND REPLENISHING THE BODY RESERVES (TO CORRECT FOR DEFICIENCIES) TO RESTORE THE UNDERLYING RESILIENCE AND ADAPTABILITY OF A HEART UNDER SIEGE
  • 6. RESTORE RESILIENCE LIGHTEN THE LOAD – BY WAY OF SAUNAS, HEAVY METAL CHELATION, SWEATING, MASSAGE, COLON CLEANSES, BLOOD DONATION REPLENISH THE RESERVES – BY WAY OF A WHOLE – FOODS, ORGANIC DIET RICH IN NATURAL FIBER SUPPLEMENTED WITH THE FOLLOWING – FISH OIL, NATTOKINASE (NATURE’S CLOT BUSTER), CoQ10, D – RIBOSE, L – CARNITINE, MAGNESIUM, L – ARGININE, VITAMIN C, VITAMIN E, VITAMIN D3, NIACITOL (A COMBINATION OF NIACIN AND INOSITOL), VITAMIN K, RED YEAST RICE, AGED GARLIC EXTRACT, LYCOPENES, BIOFLAVONOIDS, PANTETHINE, POLICOSANOL, PHOSPHATIDYLCHOLINE, GREEN TEA
  • 7. THE ADAPTABLE HEART WHEN THE CUMULATIVE IMPACT OF STRESS AND STRAIN GIVES RISE TO ISCHEMIA AND CARDIAC PAIN LIGHTEN THE LOAD, REPLENISH THE RESERVES, AND PROVIDE THE SUPPORT THE POOR HEART DESERVES IN ORDER THAT FLOW TO RESTORE, GOOD HEALTH TO REGAIN. Martha Stark (2009)
  • 8. HEART MUSCLE – FIRST AND FOREMOST A PUMP HEART – A PUMP; BLOOD VESSELS – HOSES WHEN CHALLENGED, THEY WORK HARDER IN AN EFFORT TO RESTORE HOMEOSTATIC BALANCE, THEY RESPOND TO THE CHALLENGE BY ADAPTING TO IT BUT WHEN CHALLENGED REPEATEDLY, THE HEART AND BLOOD VESSELS WILL WEAR OUT IN THE SHORT – TERM, THE STRESS RESPONSE IS VITAL IT CAN SAVE OUR LIVES BUT, IN THE LONG – TERM, IT CAN MAKE US VERY SICK STEPHEN SINATRA – STRESS IS NOT WHAT HAPPENS TO US BUT HOW WE REACT TO WHAT HAPPENS
  • 9. NARROW MARGIN OF SAFETY AND HIGH STAKES THE HEART IS PARTICULARLY VULNERABLE TO STRESS BECAUSE THE MARGIN OF SAFETY BETWEEN THE DOSE OF STRESS THAT THE HEART CAN MANAGE AND THE DOSE OF STRESS THAT IT CANNOT IS VERY NARROW AND A HEART DAMAGED BY STRESS CAN LEAD TO IMMEDIATE DEATH WITH RESPECT TO A SYSTEM AS VITAL AND VULNERABLE AS THE CARDIOVASCULAR SYSTEM, ENVIRONMENTAL STRESSORS THAT CANNOT BE ADAPTED TO WILL BE THE OCCASION FOR CARDIAC EVENTS THAT COULD WELL BE FATAL CRUCIAL THEREFORE TO SUPPORT THE HEART BY LIGHTENING ITS LOAD AND REPLENISHING ITS RESERVES
  • 10. OXYGEN UNDER RESTING CONDITIONS, MOST TISSUES IN THE BODY EXTRACT ONLY ABOUT 25% OF THE OXYGEN AVAILABLE BUT CAN ADAPT TO INCREASED METABOLIC DEMANDS BY IMMEDIATELY REMOVING A GREATER PERCENTAGE OF OXYGEN BY CONTRAST, THE HEART, EVEN UNDER RESTING CONDITIONS, ALREADY REMOVES UP TO 65% OF THE OXYGEN AVAILABLE FURTHERMORE, THE HEART HAS LITTLE ABILITY TO SUPPORT ITS ENERGY NEEDS BY MEANS OF ANAEROBIC METABOLISM AND MUST RELY HEAVILY ON ITS OXYGEN SUPPLY THEREFORE, THE PRIMARY MEANS BY WHICH MORE OXYGEN CAN BE MADE AVAILABLE TO THE HEART MUSCLE IS BY INCREASING CORONARY BLOOD FLOW BUT THE HEART CAN TOLERATE WIDE VARIATIONS IN ITS NUTRIENT SUPPLY (FATTY ACIDS, GLUCOSE, LACTATE) SO THE PRIMARY DANGER OF INSUFFICIENT CORONARY BLOOD FLOW IS NOT FUEL SHORTAGE BUT OXYGEN DEFICIENCY
  • 11. SYSTEM OF BIFURCATION LARGE BLOOD VESSELS BRANCH INTO SMALLER VESSELS, THEN INTO EVEN SMALLER ONES, AND SO ON, DOWN TO TINY BEDS OF THOUSANDS OF CAPILLARIES NO CELL IN THE BODY IS MORE THAN FIVE CELLS AWAY FROM A BLOOD VESSEL – THOUGH THE CIRCULATORY SYSTEM ITSELF OCCUPIES ONLY 3% OF THE BODY MASS THE POINTS OF BIFURCATION ARE PARTICULARLY VULNERABLE TO INJURY WITH THE CHRONIC INCREASE IN BLOOD PRESSURE THAT ACCOMPANIES CHRONIC STRESS AND INCREASED SYMPATHETIC ACTIVITY, DAMAGE BEGINS TO OCCUR AT THESE BRANCH POINTS – AND THE SMOOTH INNER LINING OF THE VESSELS BEGINS TO BREAK DOWN
  • 12. CHRONIC STRESS CAUSES PLAQUE ONCE THIS LAYER OF CELLS IS DAMAGED, THE FATTY ACIDS AND GLUCOSE THAT HAVE BEEN MOBILIZED INTO THE BLOODSTREAM BY THE STRESS RESPONSE BEGIN TO WORK THEIR WAY UNDERNEATH THIS LAYER, WHERE THEY GET STUCK, CAUSING A THICKENING OF THE LINING ALSO, DURING STRESS, THE BLOOD BECOMES MORE VISCOUS BECAUSE OF THE CLUMPING TOGETHER OF PLATELETS WHERE THERE ARE TEARS IN THE LINING OF THE BLOOD VESSELS, THESE CLUMPS OF PLATLETS WILL AGGREGATE, COMPOUNDING THE PROBLEM MOREOVER, FOAM CELLS WILL ALSO BEGIN TO GATHER OVER TIME, THE VESSELS WILL BECOME PARTIALLY OR TOTALLY BLOCKED, MAKING IT MORE AND MORE DIFFICULT FOR THE BLOOD TO FLOW
  • 13. ATHEROSCLEROSIS AND HYPERTENSION – RISK FACTORS BUT ALSO ADAPTIVE HARDENING OF THE ARTERIES AND HYPERTENSION, ALTHOUGH ASSOCIATED WITH SIGNIFICANTLY INCREASED RISK OF HEART DISEASE, ARE ALSO ADAPTIVE MECHANISMS TWO HOSES – BOTH TEN FEET TOO SHORT TO REACH THE FIRE ONE HOSE – A DIAMETER OF THREE FEET WITH SOFT, DISTENSIBLE WALLS THE OTHER HOSE – A DIAMETER OF ONE INCH WITH HARD, RIGID WALLS HARDENED ARTERIES MAKE FOR INCREASED BLOOD PRESSURE, NECESSARY TO GET THE BLOOD TO WHERE IT NEEDS TO GO BUT BOTH ARE OBVIOUSLY ADDITIONAL STRESSORS FOR THE HEART, WHICH WILL HAVE TO WORK HARDER TO GENERATE THE FORCE NEEDED TO OFFSET THE RESISTANCE OFFERED BY THE HARDENED ARTERIAL WALLS
  • 14. ATHEROSCLEROSIS AND HYPERTENSION CAN THEMSELVES PROMOTE ADAPTIVE COLLATERALIZATION HARDENED ARTERIES AND ELEVATED BLOOD PRESSURE, ALTHOUGH MAJOR RISK FACTORS, ARE THEMSELVES TRIGGERS FOR THE FORMATION OF COLLATERAL BLOOD VESSELS NATURE’S INGENIOUS WAY OF CREATING ALTERNATE ROUTES FOR OBSTRUCTED BLOOD FLOW COLLATERALIZATION, PARTICULARLY OF CORONARY ARTERIES, IS A WONDROUSLY ADAPTIVE MECHANISM EMPLOYED BY THE BODY TO RESTORE HOMEOSTATIC BALANCE
  • 15. IMPACT OF PSYCHOLOGICAL STRESS JAY KAPLAN AT BOWMAN GREY MEDICAL SCHOOL STUDIED THE RESPONSE OF MONKEYS AT THE BOTTOM OF THE TOTEM POLE WHEN IT CAME TO A SOCIAL DOMINANCE HIERARCHY MONKEYS AT THE BOTTOM OF THE HEAP ENDED UP WITH THE MOST SERIOUS ATHEROSCLEROSIS IN A VARIATION ON THIS EXPERIMENT, KAPLAN KEPT THE DOMINANCE HIERARCHY UNSTABLE BY SHIFTING THE MONKEYS INTO NEW GROUPS EVERY MONTH, SO THAT ALL THE ANIMALS WERE PERPETUALLY TENSE AS THEY JOCKEYED FOR A GOOD POSITION ON THE TOTEM POLE THE MONKEYS PRECARIOUSLY HOLDING ON TO THEIR PLACES AT THE TOP OF THE SHIFTING DOMINANCE HIERARCHY ENDED UP WITH THE MOST SERIOUS ATHEROSCLEROSIS J Kaplan & S Manuck. Status, Stress, and Atherosclerosis. Ann NY Acad Sci 1999;896:145-61.
  • 16. DEPRESSION AS RISK FACTOR “ALTHOUGH DEPRESSION AND HEART DISEASE THEY CAN AND DO OCCUR SEPARATELY, RESEARCH SHOWS THAT THE TWO CONDITIONS ARE OFTEN CONNECTED.” DEPRESSION CAN CAUSE ABNORMAL HEART RHYTHMS, INCRESED BLOOD PRESSURE, MORE VISCOUS BLOOD, ELEVATED CHOLESTEROL LEVELS, ELEVATED INSULIN LEVELS, AND ELEVATED LEVELS OF STRESS HORMONES ALL OF WHICH INCREASE THE STRESS ON THE HEART Mayo Clinic Women’s HealthSource – Feb 13, 2006. Making Connections: Depression and Heart Disease. POSTMENOPAUSAL WOMEN WITH SYMPTOMS OF DEPRESSION AND NO HISTORY OF HEART DISEASE HAD A 50% GREATER RISK OF DEVELOPING HEART DISEASE THAN DID WOMEN WITHOUT DEPRESSION S Edelstein & J Sharlin. Life Cycle Nutrition: An Evidence-Based Approach. New York, NY: Jones & Bartlett Publishers, 2008.
  • 17. THE ADAPTABILITY OF THE HEART THE HEART IS BEING CONTINUOUSLY STRESSED BY ALL MANNER OF STRESSORS (PSYCHOLOGICAL, PHYSIOLOGICAL, ENERGETIC) WHAT MATTERS WILL BE THE CUMULATIVE IMPACT OF ALL THESE STRESSORS – SYNERGISTIC, NOT JUST ADDITIVE BUT WHAT REALLY MATTERS WILL BE THE HEART’S ABILITY TO ADAPT TO THAT IMPACT IF THE UNDERLYING ADAPTABILITY OF THE HEART IS SUCH THAT IT CAN TAKE THE IMPACT IN ITS STRIDE, BY MAKING THE APPROPRIATE ADJUSTMENTS, THEN ALL WILL BE WELL BUT IF THE HEART HAS ALREADY BEEN DAMAGED, THEN THE HEART MAY BE UNABLE TO MANAGE THE STRESS
  • 18. THE OVERWHELMED HEART WHEN THE CUMULATIVE IMPACT OF STRESS AND STRAIN GIVES RISE TO ISCHEMIA AND CARDIAC PAIN IF WE LISTEN NOT TO THE MURMUR OF OUR HEART AND PRETEND THAT IN OUR FATE WE PLAY NO PART THEN OUR LIFE WE WILL NOT RETAIN. Martha Stark (2009)