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A Comprehensive Review
of Vascular Disease: Part 3Root Causes of Disease
A Peer-Reviewed Publication
Written by Charles C. Whitney, M.D.
Abstract
Evidence shows an association between oral disease
and systemic vascular disease. Physicians need our
dental colleagues’ help if we strive to optimally reduce
our patients’ risk of suffering a heart attack or stroke.
This four-part series will give dental professionals
an understanding of the pathology of cardiovascular
disease and describe how you can intervene to reduce
risk in your personal life and your patients’ lives.
Incorporating a cardiovascular health program in your
practice will elevate your credibility as a true health
professional, improve your ability to cure dental disease,
and drive the much-needed collaboration between
physicians and dentists. Part 3 of the series describes the
many root causes of vascular disease. Root causes often
make it difficult to optimally treat the direct causes
previously described. They drive disease progression
and events despite adequately controlled cholesterol,
blood pressure, and diabetes.
Publication date: June 2012
Expiration date: May 2015
Learning Objectives:
At the conclusion of this course the attendees will
be able to understand:
1. Insulin resistance, how it contributes to
vascular disease, and how it can be diagnosed
2. How sleep apnea, oral bacteria, and systemic
inflammatory disease contribute to vascular
disease
3. Other root causes of disease
Author Profile
Charles C. Whitney, M.D. is founder of Revolutionary
Health Services, www.revolutionaryhealthservices.com,
a practice established by the University of Pennsylvania
as the second concierge medical practice in the state
of Pennsylvania. He currently serves as Vice President
of the American Academy of Private Physicians, www.
AAPP.org, and has been a member of the Board of
Directors since 2007. Dr. Whitney graduated from
Jefferson Medical College in Philadelphia in 1990. He
completed his residency at David Grant USAF Medical
Center and served as a Physician in the United States
Air Force before joining the University of Pennsylvania
Health System.
Author Disclosure
The author is not compensated by any of the companies
referenced in this course.
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This course was written for dentists, dental hygienists and assistants, from novice to skilled.
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to result in the participant being an expert in the field related to the course topic. It is a combination of many
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Educational Objectives
At the conclusion of this course the attendees will be able to
understand:
1. Insulin resistance, how it contributes to vascular disease,
and how it can be diagnosed
2. How sleep apnea, oral bacteria, and systemic inflammatory disease contribute to vascular disease
3. Other root causes of disease
Roots of a plant supply the nutrients and water needed
for the parent plant to thrive. When you cut a flower off of a
plant, the roots provide nutrients to grow another flower.
Root causes of vascular disease described in this course all
feed the direct causes of disease previously discussed. Often,
high cholesterol, high blood pressure, and elevated inflammatory markers are resistant to treatment. Medications do not
effectively normalize them. A root cause may be feeding the
process to prevent their improvement. Treating direct causes
without addressing the underlying root cause is like putting
a band aid on a wound. It may feel a bit better, but it is not
healing the underlying injury.
The corollary of this is also true. If we simply treat a
root cause of disease, we will often see multiple risk factors
improve.
Hypertension has historically been called, “the silent
killer.” With good blood pressure monitors so readily available for home use, in drugstores, and at fitness centers, hypertension is no longer silent. Root causes of vascular disease
are the true silent killers. They often remain asymptomatic
and go undetected, sometimes for many years. They are the
Generals of the enemy army who send troops on stealth missions to covertly attack in the war on our life!
Insulin Resistance
Insulin resistance is the disease process that eventually leads
to diabetes. Diabetes and pre diabetes are simply statistical diagnoses, in which blood glucose is elevated. In 1997,
millions of people were diagnosed with diabetes overnight.
Why? The American Diabetes Association simply changed
the definition from a fasting blood sugar >140 to a fasting
blood sugar >125.
What is insulin resistance?
Insulin removes glucose from our circulating blood and
distributes it to tissues to be used for energy. Insulin resistance is exactly what its name implies. Insulin becomes
less effective at shuttling glucose from the bloodstream to
organs and muscles that need it.
Blood glucose levels begin to rise above normal. The
beta cells in our pancreas respond by pumping out extra
insulin to adequately lower glucose. The extra insulin
often overshoots its mark, dropping the glucose too low.
Low glucose is called hypoglycemia. Many people who
experience the hunger, cravings, fatigue, and irritability of
hypoglycemia have insulin resistance, and are actually on
the path to diabetes.
When blood glucose is low, we crave high glycemic index
foods because they are a quick glucose source. Glucose then
rises high, beginning the cycle again. This cycle is illustrated
in figure 1.
Figure 1- Insulin response to glucose fluctuations.
Modern life’s disease path
Glucose - Insulin response curve
Insulin
Blood
glucose
Baseline
insulin
Baseline
glucose
Orange
Juice
Bagel
Morning
Hamburger
Soft Drink
Candy bar
Noon
Huge meal
Evening
From Dr. A’s Habits of Health, by Wayne Scott Andersen, M.D.
As a person becomes more insulin resistant, an increasing amount of insulin is required which causes these swings
in blood glucose to widen. The amount of insulin excreted
continually rises over many years.
Eventually, the pancreas is unable to keep up with the
increasing demand for insulin, causing glucose to rise to meet
the definition of diabetes. It is thought that there may be a
15-20 year gap between the onset of insulin resistance and the
formal diagnosis of diabetes.
During this critical time between the onset of insulin
resistance and a formal diagnosis of diabetes, our circulating
insulin levels slowly rise, sometimes to very high levels, while
circulation glucose remains “borderline.” It is high levels of
insulin that drive arterial disease, not high glucose levels.1
What is the difference between Type I and Type II
diabetes?
Type I Diabetes- In Type I diabetes, the immune system
destroys all of the beta cells in our pancreas so no insulin is produced. The trigger is often unknown, but is commonly thought
to be a virus. If a type I diabetic does not take injectable insulin,
they will die. Only about 2% of all diabetics are Type I. It commonly presents in childhood and young adulthood, which is
why it was previously called childhood onset diabetes.
Type II Diabetes- Type II diabetes is diagnosed when
insulin resistance worsens enough that the patient meets one
of several criteria to diagnose diabetes. There are actually
high levels of circulating insulin in Type II diabetes.
Eventually, beta cells in the pancreas may “burn out”.
When this happens, insulin is required in order to survive,
just as in a type I diabetic. It is estimated that 2/3 of the beta
cells in our pancreas no longer function by the time a patient
is formally diagnosed with diabetes.2
2www.ineedce.com
What causes insulin resistance?
Genetics, age, lack of physical activity, and being overweight
all contribute. Abdominal fat, measured as visceral fat, is
highly contributory.
What symptoms does insulin resistance cause?
Diabetes causes excessive urination, excessive thirst, poor
wound healing, susceptibility to infection, and a peripheral
neuropathy resulting in neurologic symptoms in our extremities.
Symptoms of insulin resistance prior to diabetes are
much more subtle, often mistaken for normal aging.
Weight gain- High levels of insulin promote fat storage, particularly in our liver and around our abdominal
organs. This makes us much more prone to weight gain.
High insulin also makes weight loss more difficult because
we are less able to mobilize fat. We become a fat producing
factory.
Cravings- When glucose bottoms out as described
above, it sends a signal to our brain to seek quick energy,
typically sweets and high glycemic index carbohydrates.
Reduced energy levels- people with insulin resistance
commonly have reduced energy and excessive daytime
sleepiness. Swings in glucose levels cause difficulty focusing.
Poor sleep- Poor quality sleep and difficulty staying
asleep are common with insulin resistance.
The “Whitney Theory” of middle-aged malaise
There are many theories that speculate why people begin to
experience weight gain, fatigue, and sleep difficulties when
they reach middle age. Some theories are “slowing metabolism”, diminishing Dehydroepiandrosterone (DHEA)
a precursor to male and female sex hormones, dropping
estrogen during menopause in women, and low testosterone
causing andropause in men. Although any of these could
contribute, I strongly believe that the primary cause of weight
gain, fatigue, and sleep difficulties that many people begin to
experience during their 40s-60s, often younger, is the onset of
insulin resistance. Countless people describe increased energy, improved sleep, and much easier weight maintenance
once the overproduction of insulin is controlled.
What is the relationship between insulin
resistance and vascular disease?
The American Heart Association has declared that diabetes
is a coronary artery disease equivalent. That means that if a
person has diabetes, they should be assumed to have coronary artery disease; however, even insulin resistance without diabetes can increase your risk of heart attack and stroke.
A group of patients who had suffered a heart attack, but had
no diabetes or even elevated fasting glucose, were given a 2
hour glucose tolerance test (2 hour OGT). 66% were found
to be insulin resistant!3 Insulin resistance without diabetes
increases stroke risk as well.4
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One of the nation’s leading diabetes experts, Dr. Ralph
De Fronzo reports, “once insulin resistant, you are on a
proatherogenic path.”
Elevated insulin levels damage arteries through many
mechanisms. It worsens dyslipidemia, increases blood pressure, promotes inflammation, and causes endothelial dysfunction, all direct causes of disease. It may contribute to soft
plaque formation, making it more vulnerable to rupture.
Insulin resistance:
• Lowers total HDL and HDL2b
• Raises triglycerides
• Increases small dense LDL particles,
LDL 3a+b and 4b
• Increases Apo B
• Increases inflammatory marker Lp Plac2
• Increases inflammatory marker hsCRP
• Increases microalbumin/creatinine ratio
• Increases blood pressure
Does a patient have insulin resistance?
Is a person in that 20 year window between the onset of insulin resistance and diabetes? Here are a few clues:
• Body Mass Index (BMI) >27
• Waist >40 (men), >35 (women)
• Personal medical history- Polycystic ovary syndrome
(PCOS), gestational diabetes, preeclampsia during
pregnancy, idiopathic peripheral neuropathy, and the
skin condition Acanthosis Nigricans are all associated
with insulin resistance.
• Family history- diabetes, premature cardiovascular
death, PCOS in a sister (even if you are male)
• Native American heritage
• Erectile dysfunction
• Sleep difficulties
• High levels of central fat- either a high visceral fat
measurement or large waist circumference (the “apple”
distribution of fat)
• Gum inflammation
• High blood pressure
• Heart rate consistently above 75
• Elevated or rising uric acid
•
•
•
•
•
•
•
•
Review past blood work. There may be some clues there too:
High triglycerides
Low HDL
Fasting blood sugar >90
Hemoglobin A1c >5.6
Elevated inflammatory markers
Elevated liver tests GGT and ALT
Low vitamin D
Specifically look at the triglyceride/HDL ratio. An
elevation suggests insulin resistance (Caucasians > 3.5,
Hispanic > 3.0, Non-Hispanic blacks > 2.0)5,6
3
If there is any suggestion that a person has insulin resistance they should be tested. It is completely curable in
the early stages before significant beta cell burnout occurs.
The repercussions of ignoring it can be devastating. Curing
insulin resistance can also improve quality of life.
The American Diabetes Association defines “pre-diabetes” as:
• Fasting blood glucose > 100
• 2 hour glucose in a 2 hour OGT > 120
• Hgb A1c > 5.6
Remember that these are simply statistical diagnoses.
Insulin resistance may be present without being prediabetic.
It is impossible to determine the exact moment a person
becomes insulin resistant, but there are good ways to assess
the possibility.
Metabolic Syndrome 7- like diabetes and pre diabetes,
metabolic syndrome is simply a statistical diagnosis. It is
not a very sensitive way to find insulin resistance, but is
very specific. If a person meets 3 of the following 5 criteria
for metabolic syndrome, there is a 90% chance that they are
insulin resistant.8
1. Large waist circumference (men >40”, women >35”)
2. Triglycerides > 150
3. Low HDL cholesterol (men <40, women <50)
4. Elevated blood pressure (systolic >135 or diastolic > 85)
5. Fasting glucose >100
Waist circumference is measured at the top of the iliac
crest. If they are on medication to treat blood pressure, triglycerides, or HDL cholesterol, these criteria are considered
positive.
Sleep apnea- Dr. Defronzo reports that up to 95% of
people with obstructive sleep apnea have insulin resistance.
Insulin response improves within two weeks of initiating
CPAP.9
Fasting insulin level- The pancreas produces insulin in
response to consuming calories. After fasting for 12 hours,
there should be very little circulating insulin. The fasting
insulin level should be less than 10. Any elevation suggests
ineffective insulin functioning, requiring a higher insulin
level to keep the blood glucose low.
It would be helpful if we could measure insulin levels
after consuming calories to determine if excess insulin is
needed to process consumed energy. Unfortunately, testing
limitations and significant variability between individuals
makes postprandial insulin measurements unreliable.
2 hour OGT is the best test available outside of the
research lab to find insulin resistance at its earliest stage. In
this test, a patient fasts for 12 hours and has a glucose level
drawn. A 75 g oral glucose solution is then consumed. Glucose levels are then obtained at 1 and 2 hours after drinking
the solution. If any measurement is elevated, the patient has
insulin resistance. Fasting glucose should be <100, 1 hour
<125, and 2 hour <120. A fasting glucose >90 may signify
early insulin resistance.
It is extremely important that glucose is measured at both
1 hour and 2 hours. Some Physicians only order fasting and
2 hours measurements. In 2010, Dr. Defronzo followed over
3000 people who had a mildly elevated 2 hour glucose reading
and followed them for 7-8 years. He found that a mildly elevated fasting glucose was insignificant if the 1 hour measurement was normal. Conversely, he found that people whose
fasting glucose was <90, but had an elevated 1 hour reading
were 13 times more likely to progress to full diabetes than if
they had an elevated fasting glucose between 100-125 with a
normal 1 hour reading.10
What can be done to treat insulin resistance?
Insulin resistance is completely curable, especially during
its early stages. Once beta cells begin to burnout, it becomes
increasingly difficult to control.
The following are ways to improve insulin functioning.
• Aerobic exercise
• Interval (anaerobic) exercise
• Shut down the insulin pump through weight loss and
healthy habits of eating. The effect is almost immediate
in most people.
• Treat other root causes of disease that contribute to
insulin resistance such as oral disease or sleep apnea.
• Supplements such as chromium and cinnamon may
improve insulin function.
• Medications may be indicated, especially if vascular
plaque is present, if inflammation cannot be adequately
controlled through other measures, or if genetic testing
places them at higher risk. Genetics will be discussed in
part four of this series.
Oral health
Unfortunately, many physicians are unaware of the latest
research, and therefore underestimate the very significant association of oral health and vascular health. Physicians rarely
ask about gum disease.
I’m a physician, and I only recall one lecture about gums
and teeth from medical school. It was an anatomy class and I
remember very little. There were no discussions about teeth
and gums during residency. Many physicians regularly look
past the teeth and gums straight back to the tonsils and back
of the throat.
Over the past decade, studies have shown an unequivocal
association between oral health and vascular health. Patients
with known coronary artery disease have an increased incidence of periodontal inflammation.11 It appears that there are
at least five oral bacteria that increase the risk of developing or
worsening arterial plaque (Aa, Pg, Tf, Td, and Pi). Multiple
studies have shown the presence of these bacteria in the carotid arteries removed during carotid artery surgery!12-14 Some
4www.ineedce.com
patients in whom high levels of bacteria were found did not even
display visible evidence of periodontal inflammation, suggesting
that dental exam may be unreliable. Just the presence of these
high risk bacteria may cause disease.13
Furthermore, the simple presence of these bacteria is associated with arterial thickening seen on CIMT ultrasound.15
Most importantly, a higher incidence of heart attack is seen
when the bacteria are present in high quantities.16
It is unknown exactly why this significant association exists
between oral disease and vascular disease, but recent research
provides some clues.
The presence of causative bacteria directly increases both
systolic and diastolic blood pressure.17 Also, aggressive treatment of existing periodontal disease improves both endothelial
function and vascular inflammation.18 Lastly, multiple studies
have shown a link between periodontal disease and diabetes.
In clinical practice, the exact reason for the association between certain oral bacteria and arterial disease is not important.
It does not matter whether oral bacteria are causing arterial
disease, the bacteria are innocent guests of existing disease, or if
they accelerate existing disease.
Evidence strongly suggests that the presence of dangerous
oral bacteria is a root cause that drives insulin resistance, inflammation, high blood pressure, and endothelial dysfunction.
In order to adequately treat these direct causes of disease, oral
disease must be identified and eliminated.
Sleep apnea
Sleep apnea is a common, under-diagnosed, and often not
so silent root cause of arterial disease. It promotes insulin
resistance, high blood pressure, and inflammation making
them more difficult and sometimes impossible to treat.
Sleep apnea is when we slow or stop breathing while
sleeping. It can last for several seconds and cause blood oxygen level to significantly drop. When our body recognizes
an increased need for oxygen it pulls the fire alarm to ac-
tivate our sympathetic nervous system to drive physiologic
changes in an effort to jumpstart breathing and replenish
oxygen supply.
There are two types of sleep apnea. An uncommon cause
is central sleep apnea, a disruption of the brain’s signal to
breathe. The other is obstructive sleep apnea (OSA), which
has two causes. Excess fat as seen in obesity causes OSA
by blocking the flow of oxygen as a mass effect. Excessive
muscle relaxation in the pharynx can also cause apnea. In
such cases the tissue is floppy and falls back to block the flow
of oxygen. OSA increases during the deep stages of sleep,
and varies with sleep positions. It is most prominent when
we sleep on our back.
Most people associate OSA with obesity. Although
obesity significantly increases a person’s risk of sleep apnea,
there are many thin people with OSA whose musculature
relaxes excessively.
Sleep apnea is highly associated with arterial disease. It
has been shown to disrupt endothelial function,19 increase
inflammatory markers,20 and thicken the arterial wall.20
Effective treatment of OSA has been shown to significantly reduce cardiovascular events, and even the onset of
cardiovascular disease.21 Risk reduction appears to be
through improving multiple arterial risk factors. Insulin
resistance improves within two weeks of initiating CPAP.22
Within three months of treatment there is improvement in
Hgb a1c,23 inflammatory markers,24 and blood pressure can
significantly drop.25
Many people are averse to treating their apnea. Lack
of treatment can make it very difficult to optimally control
these other important risk factors.
OSA is much more common than most realize. It is
estimated that about 43 million Americans suffer from this
very treatable condition, 80% of whom remain undiagnosed.
Table 1 below shows the prevalence of OSA in various
medical conditions.
Table 1: Prevalence of OSA in various medical conditions
Condition
High Blood Pressure
Drug Resistant High Blood Pressure
Congestive Heart Failure
Atrial Fibrillation
Coronary Artery Disease
Stroke
Metabolic Syndrome (pre diabetes)
Type II Diabetes
Obese Diabetics
Obesity with BMI>35
Extreme Obesity with BMI>40
Acid Reflux
Simple Snoring
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% with OSA
30%
83%
85%
49%
38%
92%
50%
48%
70%
50%
98%
60%
60%
Source
Nieto- JAMA 2000
Logan- Hypertension 2001
Jiang- Journal of Cardiac Failure 2007
Gami-Nat Clin Pract Cardiovasc Med 2005
Moore-Am J Resp Crit Care Med 2001
Noradina- Singapore Med J 2005
Ambrosetti- J Cardiovasc Med 2006
Einhorn- Endocrinology Practice 2007
Brooks- J Clin Endocrinol Metab 1994
Fritscher- Obesity Surg 2007
Valencia-Flores 2000
Valipour- Chest 2002
Valipour- Chest 2002
5
Some of these statistics are staggering! Mild sleep apnea
is seen in half of everyone with atrial fibrillation, obesity,
or insulin resistance; in almost two thirds of everyone who
snores; in almost everyone who has drug resistant high blood
pressure, heart failure, and people who have suffered a stroke.
There are several clues that suggest a person has sleep
apnea. Symptoms include waking without feeling rested,
unusual daytime sleepiness, and “snorting” while sleeping.
A lesser known symptom is acid reflux (especially at night).
OSA also increases nighttime urination, and is commonly
misdiagnosed as enlarged prostate or overactive bladder.
Sleep apnea makes weight loss difficult.
• Leptins and Ghrelins are chemicals that modulate appetite. Sleep deprivation and disordered breathing while
sleeping alter their levels, increasing hunger.26
• Poor sleep makes exercise more difficult. Performance is
reduced and fatigue can reduce calorie expenditure.
• Depression is more common with sleep apnea and leads
to reduced activity and increased eating.
Tobacco Products
All tobacco products are detrimental to vascular health. The
use of smokeless tobacco is as risky for vascular disease as
smoking,27 possibly worse since the nicotine concentration is
higher.
Smoking more than 20 cigarettes a day imparts a fivefold increased risk of heart attack.27 Furthermore, smoking
significantly increases the risk of developing diabetes and
periodontal disease.28
Secondhand smoke is important too. Exposure to secondhand smoke increases the risk of heart attack by up to 25%
when compared to people not exposed to any smoke.27
Nicotine is one of the most addictive substances on the planet. Many people who have a history of alcohol and drug abuse
report that quitting smoking was the most difficult to stop.
Systemic Inflammation
Dr. Marc Penn, Cardiologist and former head of the Cleveland Clinic Heart/Brain Institute once commented, “The
only reason rheumatoid arthritis it is not considered a coronary artery disease equivalent, is that we have not proven
it yet.” By this he means that rheumatoid arthritis patients
appear to have a significantly increased risk of heart attack
and stroke compared to the general population.29
There is mounting evidence that systemic inflammation is the root cause of many common medical conditions
including vascular disease, many cancers, Alzheimer’s
disease, adult onset asthma, macular degeneration and other
ailments. Autoimmune driven inflammation contributes to
rheumatoid arthritis, vasculitis, inflammatory bowel disease, psoriasis, and others.
Humans were wired for the immune system to recognize
an enemy infection, cancer cell, or other substance that
could cause harm. It then mounts an attack to eliminate the
enemy through white blood cells, monocytes, macrophages,
cytokines and other immunomodulators. Autoimmune disease occurs when the immune system attacks normal tissue
in the absence of an invader.
It is important to assess every patient with an autoimmune
inflammatory disease for the presence of vascular disease and
the activity of vascular inflammation through monitoring of
inflammatory markers. We cannot assume that if rheumatoid
arthritis is in remission, or psoriasis is relatively inactive,
that it reflects adequate control of vascular inflammation.
A very treatable source of chronic inflammation is our
21st century pro inflammatory western culture. High fructose corn syrup, processed sugars, high glycemic index
foods, trans fats, excessive saturated fat, lack of physical
activity, and self imposed toxins like tobacco products all
perpetuate chronic inflammation that accelerates vascular
plaque deposition.
Lastly, it is important to treat comorbidities more
aggressively in any patient with chronic inflammation.
Patients with high cholesterol in addition to rheumatoid arthritis have a seven fold increased risk of heart attack. Lupus
patients with high cholesterol have an 18 fold increased risk
of heart attack.30
Other root causes of arterial Disease
The following are other conditions that may place a patient at
increased risk of having vascular disease. Research may not be
strong for all, but there is at least an association. Each should
be considered a red flag for possible disease and warrant more
aggressive risk factor screening and testing for the presence
of disease.
Erectile dysfunction- Most cases of erectile dysfunction are due to reduced flow of blood to the penis. Some is
organic, some is purely psychogenic (performance anxiety),
but most has at least a component of vascular disease. Viagra, Levitra, and Cialis all work by dilating blood vessels.
Restless leg syndrome- There is an association between restless leg syndrome and vascular disease. The connection may be poor quality sleep from sleep apnea.
Career fields- people who work intense jobs like firefighters, policemen, and emergency medical technicians
may be at increased risk.31
Migraine headaches- The reason for this association is
poorly understood, but there may be an association in both
men and women.
Psychosocial stressors- This contributor is difficult
to quantitate. Anxiety and post traumatic stress disorder
(PTSD) appear to increase risk, but depression alone does
not. Minimizing stress and anxiety are important in people
with known disease. Relaxation techniques may improve
arterial blood flow.
Post breast cancer treatment- The reason for this association is unclear. It could be from medications used to
6www.ineedce.com
treat breast cancer, or weight gain/reduced activity in post
breast cancer treatment patients.32
Use of birth control pills and hormone replacement
therapy (HRT) - There are both vascular protective and
pathogenic properties to hormonal treatments, so therapy
must be individualized. All women on post menopausal
HRT should consider taking aspirin.
History of preeclampsia- Pre-eclampsia occurs in some
women during pregnancy. Blood pressure rises significantly
and protein spills into the urine. Women with pre-eclampsia
may be at increased risk for vascular disease, even young women. Begin screening risk factors 3-6 months after delivery.33
Retinal disease- Retinopathy is most commonly associated with diabetes, but any retinopathy imparts an increased
risk of vascular disease. The more severe the retinopathy,
the higher the risk of cardiovascular death.34
Elevated uric acid- Uric acid can crystallize to cause
gout and occasionally kidney stones. There is evidence that
elevated uric acid levels is a vascular risk factor. Elevated
uric acid is seen with insulin resistance, so rising levels of
uric acid may reflect developing insulin resistance.
In the final course, you will learn how genetic testing
can be used to guide treatment of vascular risk factors. You
will also learn an approach to assessing and treating existing
risk factors. Recommendations will be made for a variety of
ways dental professionals can contribute to the war against
heart attack and strokes.
References:
1.
2.
3.
4.
5.
6.
Decode Study Group. Lancet 1999;354:617-621
DeFronzo R. Diabetes Vol. 58,April 2009
Diabetes Care, 2008 Vol. 31,no. 10:1955-59
Hoole,S.P., et al. Cirrulation 2009;119:820-827
McLaughlin, Revean, et al., Am J. Cardiol2008;96:399-204
Chaoyang Li, et al., Cardiovascular Diabetology 2008, 7:4
do::10.1186/1475-2840-7-4
7. NCEP ATPIII Circulation 9/12/2005
8. Diabetes Care 2004;27:978-983
9. Harsh et al. Am J Respir Cnt Care Med 2004;169(2):156-162
10. Abdl-Ghani, M.A., Defonzo R.A. et al., Diabestes Care 2010. Vol
33, no3:557-561
11. Corodont Study Spuhr A, et al. Arch Intern Med. 2006 Mar
13;166:554-559
12. Haraszthy VI et al. J. Renodontol 2000;71(10):1554-60
13. Gaetti-Jordim E Jr et al. J.Med Microbiol 2009;58(Pt R):1568-1575
14. Figuero E, et al. J. Periodintol posted online 3/27/2011
15. Invest Trial; Desvarieux, M. et al. Circulation 2005;111:576-582
16. Stein, J. M., et. al. J Periodontol 10/2009; 80:1581-1589.
17. Tonetti, M.S. et al., N Engl J Med 2007;356:911-920
18. Tonetti MS, et al., N Engl J Med 3/1/2007; 356:911-920
19. Kohler et al. Am J Respir Cnt Care Med 2008;178:984-988
20. Minoguchi K, et al. Am J Respir Cnt Care Med 2005;172:625-630
21. Perker Y, et al. Am J Respir Cnt Care Med 2002;166(2):159-165
22. Harsh et al. Am J Respir Cnt Care Med 2004;169(2):156-162
23. Babu AR et al. Arch Intern Med 2005;165:447-452
24. Ishida K et al. Chest 2009;136:125-129
25. Becker HF et al. Circulation 2003;107(1):68-73
26. Patel SR; Palmer LJ; Larkin EK et al. SLEEP 2004;27(2):235-9.
27. Lancet 2006;368:647-658
28. JAMA 2007;vol 298,no.22:2654-2664
29. Sodergren A, et al. Ann Rheum Dis 2007 Feb;66(2):263-6.
30. Fischer LM et al. Am J Cardiol 2004;93:198-200
31. Katessn et al. New Engl J Med 2007;356:1207-1215
32. J Am Coll Cardiol 2007; 50:1435-1441
33.British Medical Journal doi 10.1136/bmj 39335.385301.BE
11/1/2007
34. Foster J.P. et al. Heart March 2009; 95(5):391-4
Author Profile
Charles C. Whitney, M.D. is founder of Revolutionary
Health Services, www.revolutionaryhealthservices.com, a
practice established by the University of Pennsylvania as the
second concierge medical practice in the state of Pennsylvania. He currently serves as Vice President of the American
Academy of Private Physicians, www.AAPP.org , and has
been a member of the Board of Directors since 2007. Dr.
Whitney graduated from Jefferson Medical College in
Philadelphia in 1990. He completed his residency at David
Grant USAF Medical Center and served as a Physician in
the United States Air Force before joining the University of
Pennsylvania Health System.
Disclaimer
The author is not compensated by any of the companies
referenced in this course.
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Notes
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Questions
1.Which of the following is NOT a root
cause of vascular disease that feeds all the
direct causes?
a.Diabetes.
b.Inflammation.
c. Sleep apnea.
d. High risk oral bacteria.
e. Rheumatoid arthritis
2.Which of the following statements is true
about insulin resistance?
a. With insulin resistance, beta cells in the pancreas
respond by pumping out extra insulin.
b. The severity of insulin resistance cannot be
estimated by blood glucose level.
c. A person may be insulin resistant for up to 20 years
prior to the formal diagnosis of diabetes.
d. Symptoms of low blood sugar may actually suggest
the presence of insulin resistance.
e. All statements are true.
3.Which of the following statements are
true about early type 2 diabetes?
a. The pancreas stops producing insulin.
b. High levels of insulin are excreted
c. Many beta cells in the pancreas may become
nonfunctional by the time the diagnosis is made.
d. Diagnosis is typically made in young adulthood.
e. Both B and C.
4.Which of the following is NOT a risk
factor for type 2 diabetes?
a. Increasing age.
b. Sedentary lifestyle.
c.Obesity.
d. High visceral (abdominal) fat in the absence of
being overweight.
e. All of the above are risk factors.
5.Which of the following statements is
NOT true about insulin resistance?
a. People are prone to weight gain because of both
increased fat storage and difficulty mobilizing fat.
b. Many people experience cravings for sweets and
high glycemic index carbohydrates.
c. Glucose fluctuation causes reduced energy and
difficulty focusing.
d. It causes increased quantity of sleep.
e. All of the above statements are true.
6.Which of the following statements is
NOT true about insulin resistance?
a. Diabetes should be considered a coronary artery
disease equivalent.
b. Insulin resistance, without diabetes increases,
stroke risk.
c. Insulin resistance, without diabetes increases heart
attack risk.
d. Most people who suffer a heart attack are insulin
resistant.
e. All of the above are true.
7.Which of the following is NOT a
laboratory change with insulin resistance?
a.
b.
c.
d.
e.
Increased small dense LDL particles.
Increased APO B
Increased inflammatory markers.
Increased HDL2b cholesterol.
Increased microalbumin/creatinine ratio
8.Which of the following is NOT a clue
that a person may be developing insulin
resistance?
a.
b.
c.
d.
e.
Body mass index of 28.
A woman with a waist measurement of 36 inches.
A developing neuropathy.
Developing high blood pressure.
All of the above may suggest developing insulin
resistance.
9.Which of the following is a criterion to
diagnose prediabetes as defined by the
American Diabetes Association?
a. Hemoglobin A1c of 5.7
b. A two-hour reading of 110 during a two-hour oral
glucose tolerance test
c. A man with a waist circumference of 41 inches.
d. Fasting glucose of 99
e. Vitamin D <30
10. Which of the following statements are
true about metabolic syndrome?
a. It is a sensitive method to assess for insulin
resistance
b. 90% of people who meet 3 of the 5 criteria are
insulin resistant
c. Waist circumference is measured at the navel.
d. A and B
e. All of the above are true
11. Which of the following are true about
a two-hour oral glucose tolerance
(OGT) test
a. A fasting glucose <90 is always reassuring
b. An one-hour reading is not usually necessary.
c. An elevated fasting glucose is the most important
criteria.
d. A mildly elevated fasting glucose may be
insignificant. If the one hour measurement is
normal.
e. A, B and C are true
12. Which of the following statements is true
about high risk oral bacteria?
a. Aa, Pg, Tf, Td, and Pi have been shown to be high
risk for developing systemic disease.
b. The presence of high risk bacteria are associated
with arterial thickening seen on CIMT ultrasound.
c. Some patients with high levels of high risk bacteria
do not show visible evidence of inflammation on
dental exam.
d. A and B only
e. All of the above
13. Which of the following statements are
true about the oral-systemic link?
a. Aggressive treatment of existing periodontal
disease improves vascular inflammation.
b. Aggressive treatment of existing periodontal
disease improves endothelial function.
c. The presence of causative bacteria increase both
systolic and diastolic blood pressure.
d. The presence of high levels of causative bacteria
increase risk of heart attacks and strokes.
e. All of the above
14. Sleep apnea may cause all of the
following EXCEPT
a.
b.
c.
d.
e.
High blood pressure.
Systemic lupus erythematosus.
Insulin resistance.
Restless leg syndrome.
Elevated hsCRP inflammatory marker
15. Which of the following is NOT a true
statement about sleep apnea
a. Central sleep apnea is a result of a disruption in the
brain and signal to breathe
b. Severity of sleep apnea varies by position of sleep.
c. Achieving an optimal body mass index of < 25 will
cure sleep apnea
d. Sleep apnea contributes to arterial disease by
disrupting endothelial function, increasing
inflammatory markers, and thickening the arterial
wall.
e. All of the above are true.
16. Which of the following physiologic
changes are seen within 3 months of
treating sleep apnea with CPAP?
a.
b.
c.
d.
e.
Improved insulin resistance.
Improved hemoglobin A1c
Improved inflammatory markers.
Improved blood pressure.
All of the above
17. Which of the following statements about
the incidence of sleep apnea is NOT true?
a. 60% of people who snore have sleep apnea.
b. 80% of people with drug-resistant hypertension
have sleep apnea.
c. 50% of people with metabolic syndrome have sleep
apnea.
d. 60% of people with acid reflux have sleep apnea.
e. All of the above are true
18. Which of the following are true
statements about sleep apnea?
a. Nighttime urination is often misdiagnosed as
enlarged prostate in men.
b. Treatment may improve acid reflux.
c. Leptin and Gherlin levels are altered which
decreases appetite.
d. A and B only
e. All of the above
19. Which of the following statements about
the use of tobacco products is NOT true?
a. Cigarettes are a higher risk than smokeless tobacco
b. Smoking more than 20 cigarettes daily imparts a 5
fold increased risk of heart attack.
c. Secondhand smoke increases the risk of heart attack
by up to 25%.
d. Nicotine concentration is higher in smokeless
tobacco than in cigarettes.
20. Which of the following are possible root
causes of arterial disease?
a. Erectile dysfunction
b.Anxiety.
c. Post breast cancer treatment.
d. Migraine headaches
e. All of the above
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ANSWER SHEET
A Comprehensive Review of Vascular Disease:
Part 3- Root Causes of Disease
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A Division of PennWell Corp.
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