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Primal Health/Nutrition Expert > Chapter 6 - Fat & Cholesterol Are Not Your Enemy > Flashcards

Chapter 6 - Fat & Cholesterol Are Not Your Enemy Flashcards

1
Q

The true catalysts for heart disease

A

Oxidation
Inflammation

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2
Q

Cholesterol

A

A waxy molecule composed of lipid fat

Contained in the membrane of every cell in the body, as well as blood plasma.

Critical to:
- Building and maintaining cell membranes
- Metabolizing fat-soluble vitamins
- Producing bile to help digest fat
- Synthesizing hormones, including sex hormones

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3
Q

Endogenous Production of Cholesterol

A

Manufactured in the liver, which varies in accordance with dietary intake

And virtually all cells in the body can manufacture cholesterol (or pull more LDL from the bloodstream) if insufficient levels are detected in the cell…

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4
Q

Lipoproteins
(Lipid-protein)

A

Carries oil-based cholesterol and other fats (triglycerides, phospholipids) through the water-based bloodstream.

Several varieties, with different transportation functions, that comprise the total amount of cholesterol in the body.

*each carries a certain percentage of cholesterol, triglycerides, and other minor fats

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5
Q

Lipoprotein types

A

In order of size, from largest to smallest:
- Chylomicrons
- VLDLs
- LDLs
- HDLs
(as well as subtractions of each)

Most promenant to heart disease = VLDLs, LDLs and HDLs (very low-density, low-density, high density)

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6
Q

HDLs (high-density lipoprotein)

A

Takes oxidized cholesterol from the bloodstream back to the liver for excretion or recycling

Comprises about 30% of the total cholesterol in a healthy body

Known as “natures garbage trucks” for their ability to cleanse the arteries and bloodstream of oxidized cholesterol

  • Has anti-inflammatory and antioxidant properties
  • Associated with a reduced risk of atherosclerosis
  • Low levels is associated with Metabolic Syndrome
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7
Q

VLDLs (very-low-density lipoproteins)

A

Manufactured in the liver to transport triglycerides and cholesterol to target fat or muscle cells

Comprised of 80% triglyceride

After delivering their cargo to target cells in the body, they shrink in size and transform into either large, fluffy LDLs or small, dense LDLs

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8
Q

Large, fluffy LDLs
(Type A)

A

Formed from VLDL when blood levels of triglycerides and insulin are low

Known as buoyant LDL

Generally harmless, even in high concentrations… however, in the presence of other risk factors
- high-insulin producing diet
- systemic inflammation
- abdominal obesity
- family history of dyslipidemia
- smoking
- etc.
even large, fluffy LDL can make a contribution to heart disease if the particle count is high enough and it’s not being cleared from the blood quickly enough.

With other risk factors:
- Low HDL (clears oxidized cholesterol from the bloodstream)
- Poor thyroid function (down-regulates LDL receptors)
—> causing LDL to circulate for longer in the bloodstream with insufficient antioxidant protection…
- and adverse lifestyle practices present,
these LDLs can circulate in the blood for too long and become oxidized

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9
Q

Small, dense LDL
(Type B)

A

Can become lodged onto the endothelial cell layer - the cells that like the walls of your arteries
- since oxygen is always traveling through the blood vessels those trapped in the endothelium can sustain oxidative damage and trigger an immune response that can progress toward an eventual heart attack

*the act of being oxidized decreases LDL size (so it’s possible that they are already partially oxidized…)

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10
Q

Health conditions and lipoprotein conversion

A
  • Insulin resistance produces excess VLDL, which converts to small, dense LDL
  • Inflammation and elevated triglyceride levels in the bloodstream (hallmarks of metabolic syndrome), increases rate of conversion

*in turn high concentrations of small, dense LDL can cause an inflammatory reaction, which exacerbates metabolic syndrome - creating a dangerous cycle of disease

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11
Q

LDL-C

A

Term for the total amount of cholesterol someone is carrying
—> (total passengers in vehicles on the road)

*the standard lipid panel a doctor orders

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12
Q

LDL-P

A

The number of LDL particles in the blood
—> (total number of vehicles on the road

*large, fluffy LDL (buses) often represents the cholesterol increase read on individuals on a high-fat paleo/primal/keto diet. These are less likely to get stuck and oxidized in the bloodstream… but a standard lipid test doesn’t show you this - an advanced lipid test can confirm that the actual particle number hasn’t significantly increased and that the change is primarily due to large, fluffy LDL

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13
Q

Atherosclerosis

A

When plaque forms in the lining of artery walls (endothelium)

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14
Q

Endothelium

A

Artery wall - one cell thick

Can become damaged due to:
- inflammation
- high blood pressure
- high blood sugar (hyperglycemia)
… among other factors

*when damage occurs, small, dense LDL can get lodged in the damaged tissue, where they are exposed to oxygenated blood (hemoglobin) passing through arteries - this constant oxidative exposure causes the area to become inflamed

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15
Q

Hemoglobin

A

Oxygenated blood

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16
Q

Foam Cells

A

Macrophages that become overwhelmed in their well-intended effort to engulf oxidized LDLs in the endothelium
- in their efforts to mitigate the damage, they expand in size
- This cell formed through the process produces a chemical called myeloperoxidase, further oxidizing the LDL particles
- These cells also release chemicals called cytokines into the bloodstream, which attract more macrophages to the area to cause more inflammatory damage…

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17
Q

Myeloperoxidase

A

Chemical produced by foam cells that further oxidizes LDL particles caught in the endothelium…

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18
Q

Cytokines

A

Chemicals released by foam cells into the bloodstream, which attract more macrophages to the inflamed area causing more inflammation…

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19
Q

Macrophages attempt to engulf oxidized LDL

A
  • A “fatty streak” appears in the artery wall.
  • Over time, this fatty streak can progress into an atherosclerotic plaque.
  • As oxidation and inflammation continue, the plaque becomes stiff and calcified and more susceptible to rupture.
  • Once rupture occurs, it can block the artery on the spot, or more commonly detach from the wall, drift into circulation, and eventually cause a heart attack or stroke
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20
Q

Cholesterol’s Role in Atherosclerosis

A
  • In a healthy body, cholesterol acts as a temporary band-aid to cover lesions in the ECL
  • When inflammation subsides, the cholesterol leaves the now-healed lesion and is recycled back to the liver by HDL

*problems arise only when inflammation is chronic and the LDL particles become oxidized…

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21
Q

Heart Disease Catylsts

A
  1. Hyperinsulinemia
  2. High triglycerides
  3. Excess cortisol
  4. Insufficient HDL
  5. Poor diet
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22
Q

Hyperinsulinemia

A

Chronically elevated insulin levels

Promotes systemic inflammation in the body
- This causes damage to the delicate endothelium by reducing the bioavailability of nitric oxide (a compound that keeps blood vessels relaxed) and
- Promotes platelet adhesiveness (sticky platelets that clot more readily)
—> these conditions increase the sheer force of blood flowing against the blood vessel walls and facilitates oxidation of small, dense LDL in endothelial lesions

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23
Q

Nitric Oxide

A

A compound that keeps the blood vessels relaxed

Bioavailability reduced in hyperinsulinemia

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24
Q

High triglycerides

A

Signal an excess of energy…

Associated with risk of:
- atherosclerosis
- heart attack
- stroke

Elevated in people with:
- type 2 diabetes
- metabolic syndrome
- hypothyroidism

Comes from:
- dietary fat
- created from glucose by the liver & adipose cells = lipogenesis

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25
Q

When liver glycogen stores are full

A
  • The liver then converts excess glucose to triglycerides
  • Triglycerides are then transported by VLDL into cells throughout the body

*in healthy individuals, about 60% of ingested glucose is transported to the liver and glucose is converted glycogen here for storage in muscle tissue and liver

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26
Q

Excess Cortisol

A

Promotes inflammation

Chronically elevated levels produce:
- poor eating habits
- chronic exercise habits
- insufficient sleep

*believed to be a driving factor in assorted health problems, cancers, and heart disease

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27
Q

Insufficient HDL

A

Can significantly increase heart attack

Due to:
- poor eating habits
- poor exercise habits
- use of statins

28
Q

Poor diet and increased risk of heart disease

A

Due to:
1. Excess carb intake & insulin production
2. Excess consumption of PUFA oils
- inherently prone to oxidize and become incorporated into LDL particles
3. Any consumption of chemically altered trans or partially hydrogenated fats
- which impairs blood flow
4. Insufficient intake of antioxidant
- help prevent oxidation in the first place
5. Insufficient intake of saturated fat
- helps elevate HDL and makes LDL particles more resistant to oxidation
6. Poor LDL clearance
- diet likely contributes to poor thyroid function, which inhibits LDL clearance

29
Q

Comprehensive Blood Testing for Heart Disease Risk (range of complexities providing big picture analysis)

A
  1. Triglycerides-to-HDL ratio
  2. Blood pressure
  3. Vitamin D
  4. Fasting blood insulin
  5. HbA1C
  6. Triglycerides
  7. High-sensitivity C-reactive protein (hs-CRP)
  8. IL-6, or Interleukin-6
  9. Homocysteine
  10. Creatine phosphokinase (CPK)
  11. Lipoprotein(a)
  12. LpA2
  13. Apolipoprotein
  14. LDL particle size/advanced lipid profile testing
  15. Coronary calcium testing
30
Q

Triglyceride-to-HDL ratio test

A

Desirable ratio = 3.5:1 or below
Superior ratio = 1:1

*Ratio of triglyceride to HDL is agreed by experts to be the most important blood metric for measuring heart disease risk…

31
Q

Excessive triglycerides are driven in part by:

A
  • excessive carbohydrate intake
  • excessive insulin production
  • conversion of excess ingested carbs into triglycerides in the liver

*high triglycerides indicate the body’s cholesterol processing system is overwhelmed

*sufficiently high levels of HDL can effectively remove potentially dangerous small, dense cholesterol molecules…
hence, for many people, elevating HDL and reducing triglycerides is a worthwhile tandem goal to reduce heart disease risk

32
Q

Vitamin D test

A

Should be assessed by a serum 25(OH)D test

Sufficient/optimal vitamin D levels:
- 50 nmol/L (20ng/mL) = a safe minimum target
- 2011 Endocrine Society concluded that a serum 25(OH)D level >75 nmol/L (>30ng/mL) = optimal

*if you are below 30ng/mL, you should consider aggressive action to get more sunlight and/or supplement

33
Q

It is possible to develop problems with excessive vitamin D levels

A

Especially, if you are deficient in vitamin A…
Synergist = potassium + vitamin K
— it’s imperative these levels are optimal if taking vit-d supplements

34
Q

Best source of vitamin A

A

Animal products, especially liver

*heavy sun exposure can deplete vitamin A, so insure you get enough by eating animal products, or at least cod liver oil…

35
Q

Toxicity concerns with Vitamin D

A

125-150mmol/L (50-60ng/mL) range
- Only happens in unique, sensitive individuals from supplementing over long periods of time
- Impossible to happen from sun exposure, since the body automatically regulates vitamin D production by tanning the skin (consequently shutting down further vitamin D production)
- Diet will not provide nearly enough vitamin D to put you into the excess zone

36
Q

Fasting Insulin Test

A

Optimal levels:
1. Dr Rickard Maurer:
- 3-8 uIU/mL (18-48 pmol/L)
2. Some functional practitioners:
- 10 uIU/mL (>60 pmol/L) as an upper limit — values above this range represent different degrees of insulin resistance

*Almost never ordered, because fasting glucose tests are…

37
Q

HbA1C

A

Measures how much glucose is attached to a hemoglobin

A reliable marker for average blood glucose levels over an extended time period of two to three months

  • Under 5.7% (39 mmol/mol) = normal
  • 6.5% (48 mmol/mol) or higher = diagnostic for diabetes
  • The intermediate range = pre-diabetic state
38
Q

Triglyceride test

A
  • Under 150mg/dL = essential to reduce disease risk
  • Under 100mg/dL = optimal
  • A reading of over 150mg/dL suggests an excess of oxidized LDL and thus, elevated disease risk
39
Q

High-sensitivity C-reactive protein
(hs-CRP)

A

A high level in your blood is a reliable sign of inflammation in the blood vessels, in the absence of acute infection…

  • Under normal circumstances or over the long-term ideal CRP = well under 1mg/L
  • Between 10mg/L - 40mg/L (and perhaps 1-9mg/L) = systemic inflammation (or pregnancy)
    —> while anything above that is associated with a serious acute condition:
  • heart attack
  • major infection
  • post-marathon or Ironman triathlon

*excess belly fat is often an indicator of C-reactive protein and systemic inflammation

40
Q

Elevated levels of hs-CRP are associated with:

A
  • increased risk of heart attack
  • increased risk of stroke
  • sudden cardiac death

*infection or acute stressors can temporarily elevate levels (and other markers of cardiac and musculoskeletal stress)
- blood levels after a marathon, for example, which should subside within 72 hours

41
Q

IL-6
(Interleukin-6)

A

Secreted by both T-cells & macrophages as part of an inflammatory response…
Therefore, elevated levels indicated systemic inflammation

42
Q

T-Cells

A

A type of white blood cell that play a huge role in the immune response

43
Q

Macrophages

A

Cells that engulf and digest (also known as phagocytosing - stray tissue pathogens

44
Q

Homocysteine

A

An amino acid that when elevated can increase risk of:
- heart attacks
- strokes
- blood clots

*vitamin and mineral deficiencies can lead to elevated levels too, making homocysteine a good general health marker to track

45
Q

Creatine Phosphokinase (CPK)

A

An enzyme found in:
- brain
- lungs (CPR-1)
- heart (CPR-2)
- skeletal muscle (CPR-3)

Elevated levels indicate damaged tissues from a medical incident or extreme athletic stress

46
Q

Lipoprotein(a)

A

Promotes coagulation (clotting), making it a heart disease risk marker

Elevated levels are strongly associated with early and aggressive forms of heart disease

47
Q

LpA2

A

An enzyme that promotes oxidation of lipoproteins, making it a heart disease marker

48
Q

Apolipoprotein B (ApoB)

A

Measures a protein residing in all LDL particles

High levels indicate elevated LDL particles number and elevated heart disease risk

*keep in mind that ApoB readings can fluctuate from day to day - retest regularly for an accurate reading

49
Q

LDL particles size/
Advanced lipid profile test

A

Examples:
- Berkeley Heart Lab test
- VAP test (Vertical Auto Profile)
- NMR (Nuclear Magnetic Resonance) test

50
Q

Coronary Calcium Test

A

Measures calcium buildup in arteries via CT scan

A strong indicator of atherosclerosis

Values are assigned an Agatson score, correlated with a cardiac mortality risk percent value

51
Q

Statin Side Effects

A
  • Suppress the production of cholesterol in the liver (all forms, including HDL)
  • Thus, it can interfere with healthy serotonin balance (less energy and alertness, and potential mood consequences)
  • Hamper with Vitamin-D synthesis
  • Cause difficulty regulating blood sugar
  • Disturbs an assortment of critical hormonal processes
  • Has been shown to cause inflammation in the liver
  • May deplete cells of a critical energy-producing nutrient known as coenzyme Q-10 (CoQ10) —> which can lead to hampering the ability of all cells to fight off free radicals and moderate inflammation, and adverse lifestyle practices (insufficient exercise)

*Have no effect on triglyceride levels of LDL particle size

52
Q

Statins have been shown to:

A
  • Anti-inflammatory effect
  • Blood thinning effect (help reduce plaque formation in those susceptible)
  • Plaque stabilizing effect (reduce risk of rupture in those susceptible)
53
Q

Chemically Altered (trans) Fats + Partially Hydrogenated Fats

A
  • Create destruction at the cellular level, by promoting systemic inflammation
  • Interfering with hormone signaling
  • Compromises immune function
  • Damages the nervous system
  • Damages the cardiovascular system
  • Damages the endocrine system
  • Damages the brain
54
Q

Most Offensive Sources of Polyunsaturated Fats

A

Vegetable oils (canola, corn, soybean, safflower, etc.)
- Easily oxidized by light, heat, or oxygen

Thus, disrupting:
- Healthy hormone and immune function upon ingestion

55
Q

Omega-3 Fats are health promoting

A

Largely due to their anti-inflammatory effect…
Lauded for enhancing:
- cardiovascular function
- brain function
- skin
- immune function

56
Q

Monounsaturated Fats are also regarded as healthy

A

Found in:
- macadamias
- avocados
- olives
- extra-virgin olive oil

Enhances
- Cardiovascular function
- Immune function
- Help protect against heart disease

57
Q

Saturated Fat

A

Bulk found in animal products
- meat (contains about equal proportions of saturated and monounsaturated fat)
- high-fat dairy

  • comprises about half of our cell membranes
  • contributes to a variety of healthy metabolic and hormonal processes
  • an abundant source of important vitamins (K2, A, and D)
  • is easily burned as free fatty acids in the bloodstream

*in the absence of high carbohydrate intake and other stress factures, saturated fat is an efficient, clean-burning energy source for the body

58
Q

When fat is consumed in the context of a high-carbohydrate diet

A

The excess insulin production promotes high oxidative stress and inflammation, along with high triglycerides
- These are the key risk factors for atherosclerosis

*when carbohydrate intake is minimal, however, dietary fat is easily mobilized as a stable and long-lasting energy source

59
Q

Epidemiological Studies

A

The study of how diet and lifestyle practices affect health

60
Q

Respected Epidemiological Studies have shown

A

No correlation between dietary fat intake or cholesterol intake and heart disease

61
Q

Palmitoleic Acid

A

Critical blood level marker for unhealthy fat storage and metabolic syndrome…
- increased levels in a study where carbohydrate intake was increased - it increased in close correlation with increased carb intake

*another study revealed that even when subjects doubled, or tripled their saturated fat intake, blood levels of fat did not increase

62
Q

Heart Disease Process

A
  1. Damage occurs to the endothelium, due perhaps to high blood pressure, high blood sugar, or smoking, for example
  2. Small, dense LDL particles (likely already oxidized) lodged in the damaged endothelium and are further oxidized by the constant flow of hemoglobin in the artery
  3. The immune system sends macrophages to the inflamed area. Macrophages become overwhelmed and convert to foam cells. Clots form and plaque accumulates
  4. Plaque ruptures, causing a stroke or heart attack
63
Q

Heart Disease Catalysts

A
  1. Excess insulin (from high-carb diet). Promotes:
    - inflammation
    - stiff arteries
    - sticky platelets
    - oxidized small, dense LDL
  2. High triglycerides (often from a high-carb diet). Promotes:
    - conversion of VLDL into small dense LDL instead of large, fluffy LDL
  3. Excess cortisol (from poor diet, chronic exercise, insufficient sleep, emotional stress). Chronic stress promotes:
    - inflammation
    - damage to the sensitive endothelium
  4. Insufficient HDL (from poor diet, statin use, chronic exercise).
    - body is less efficient at clearing oxidized cholesterol from the bloodstream
64
Q

Markers of Chronic Inflammation

A
  1. IL-6
  2. C-reactive protein
  3. Homocysteine
  4. CPK
65
Q

Three main reasons fat has been inaccurately maligned by conventional wisdom:

A
  1. Failure to distinguish between healthy and unhealthy fats
  2. Deleterious influences of a high-carbohydrate diet
  3. Propaganda and flawed science
66
Q

Reconciling opposing beliefs about diet involves:

A
  • acknowledging common ground
  • recognizing that almost any departure from the SAD diet is a step in the right direction health wise

*instead of being overwhelmed with conflicting advice, experiment for yourself and see how you feel

67
Q

Coenzyme Q-10
(CoQ10)

A

Helps the mitochondria produce energy in the cells

Depletion can result in:
- fatigue
- muscle pain
- hamper the ability of cell’s to fight free radicals
- hamper with the cell’s ability to moderate inflammation
- adverse lifestyle practices (due to low energy and pain)
- elevated oxidative damage in cells whose normal energy production mechanisms are compromised

*can be depleted due to statin intake

Primal Health/Nutrition Expert (9 decks)

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