Showing posts with label Track Your Plaque. Show all posts
Showing posts with label Track Your Plaque. Show all posts

Wednesday, December 24, 2008

Shrinkage 101 (With Vitamin D)

Here is a post...tongue-in-cheek from our wonderful community on the Track Your Plaque forum from about a year ago (when I joined). How is shrinkage desirable on many levels? Vitamin D assists on reducing many things pertinent to plaque:
--coronary atherosclerotic plaque (and elsewhere, like the penile vasculature)
--belly fat, WAT (white adipose tissue)
--small dense LDL (atherogenic particles)
--small dense HDL (atherogenic particles)
--hypertensive tension in the circulation (perfect BP: 115/75 according to TYP)
--systemic inflammation
--autoimmune-related hypersensitivity


Just a note about the TYP Forum...Several categories exist with threads on-going. I believe there is a utility for a 'Newbie's Corner' for all the new members joining us. TYP is rather overwhelming in the beginning. Right? Please don't hesitate to inquire for any help. There are many helping hands!

**General Discussion
This forum is for topics of all types for all members.

**What Else is New? Interesting Finds from Other Places
This is the place to post interesting heart health news that you wish to share with other Members.
**Track Your Plaque 101 - Basic Q&AThis is the forum for basic questions about the Track Your Plaque Program and heart disease prevention and reversal. Questions should be short, specific, and of a nature that can be answered quickly so that our staff can address as many as possible. Questions will be prioritized on this basis. Please keep in mind that it is illegal to diagnose or prescribe treatment over the Internet. Replies are designed to be of a general nature and not meant to treat a specific individual or replace the advice of your physician.

**Advanced Discussion Forum
This forum exists to collect input and questions on advanced topics about heart disease, lipoproteins, prevention and regression. This forum is monitored for items of interest for upcoming articles and developing the Track Your Plaque program. Questions are typically not answered directly but may be answered generally if there is common interest among contributing members.

**Emerging Medicine
This is the forum for discussions and information on new and experimental heart disease theories and treatments. It was added by Member request to relieve the burden on the Advanced Discussion Forum and to provide easy access to posts on what the future may hold for heart disease prevention, detection, reversal, and cures.
**Who do you trust?Unfortunately, trusted sources of reliable heart health information can be darn hard to come by. Tell other Track Your Plaque Members about the doctors, scan centers, and other sources of information, products, and services that you've come to trust and have been helpful to your plaque control program.

**Tell us your story
Tell us about your successes, failures, horror stories, or come here to just converse with other Track Your Plaque Members. We love your testimonials!
**Recipe RepositoryMembers have asked for a place to share their favorite heart healthy recipes. This is it! In order to maintain uniformity please use the following format. Recipe Name, Short Description, Ingredient List (amount, unit of measure, description), preparation instructions, comments. Bon Appetite!




ggglll Posted: 1/26/2008 9:48:00 AM

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I love classic Seinfeld...

Do you 'member the episode with George and shrinkage??!
(the accidental full Monty... and cold... *HEEEE HEEEE*)



Women are in the same boat, we have shrinkage as well... Sadly... and it has to do with vitamin D!

http://mend.endojournals.org/cgi/content/full/18/9/2208
Accelerated Mammary Gland Development during Pregnancy and Delayed Postlactational Involution in Vitamin D3 Receptor Null Mice



Gals, recall after breastfeeding when the mammary glands (ie, b**bies -- can I say that here?) minimized from obscene-XXX sizes to negative(-)A's?

VDRs (vitamin D receptor and vit D) return them to non-lactating form (and rather hanging to the knees, shriveled like raisins; no one is upset... or in need of plastic surgery).

Of course, here on TYP, SHRINKAGE is the optimal outcome!!! PLAQUE shrinkage is a G-O-O-D thing (as well as colon, prostate, ovarian and breast cancer).

(another D E E P thought...)
(from the shallowest-thinking member)




DR. Davis' Comment
Posted: 1/27/2008 9:58:00 AM

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Hi, G-- I believe that the authors' comment that vitamin D "is best known for its role in maintenance of calcium homeostasis, 1,25-(OH)2D also regulates epithelial cell proliferation, differentiation and apoptosis" is most telling. I remain very excited about the plaque-regressing, calcium-normalizing, and cancer-preventing properties of this fascinating hormone/nutrient.
----------------- Dr. William Davis Author, Track Your Plaque




Anonymous Posted: 1/28/2008 4:22:00 PM

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g It shrinks? "YES, like a frightened turtle!" I don't know how you guys walk around with those things! Good luck with the vitamin D. Wonder if that's what Pamela Anderson used, and if so how many IU's of D per day



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P.S.
2009 update on the uummm mammaries...thanks to vitamin ADEK/TYP/hyperlipid/Paleo diet there is sustainable growth without unwanted shrinkage I'm glad to report (I suspect the synergy betw Vitamin D and Vitamin A and mod/high-fat-diet has improved my ummm...34-24-34 numbers the most).

Incidentally, the HDLs are up from 84 to 89 now (27% incr from 70 baseline) and body fat down to 19.5% (from 22%) (despite hormone issues and mild vit D insufficiency [25(OH)D]). I'm trying to beat Richard *hee* here at Free the Animal (HDL 104) and Stephan here at Whole Health Source (!! wow !! HDL 111). What brilliant beasts! OMG... wtf how amazing are these measurements... Of course these lab values (incl mine) are all Freidewald calculations -- and thus liable for some miscalculations and inaccuracies by ~10% or more (the lower the HDL, the more inaccurate, imo; the larger, too? I dunno?).

I'll show you how the new TYP tracking graphics work in a few wks...wow...they are beautific and will blow your mind... (after more shrinkage *ah haa* and better ABS and labs) !

Monday, November 3, 2008

Dead and Gone...the Old Me

When you've stepped into a new realm of extreme longevity and optimal fitness and health, how do you feel?

Like the old self is gone?

When I attend weddings for relatives and old friends, it's seriously scary/odd how people don't recognize you. Because internally you are the SAME person, but physical transformations can be overwhelmingly out of proportion. Blown away. Can't comprehend. No one has any idea that a more vital, energy-filled, blasting life can be awaiting them.

Movement with a little intensity, vitamin D/A/E/K, fish oil, seafood/grassfed meat, omega-3 eggs, wheat-free (semi-dairy/legume-free), low carb is the only way to go. It's not hard. At ALL. In fact, it's purely incomprehensibly curious to NOT engage in this T.Y.P. HEDONIA-lifestyle.

The Old Me...GONE...certainly that's how I feel now -- engaged a year now...! Yep, been about a year on TYP and can't imagine feeling how lethargic, slow, sluggish, mentally fogged I was before. Asthmatic, scratchy skin, poor reflexes, SAD (seasonal affective disorder), cold extremities like semi-Reynaud's, and the list goes on-and-on... Beyond one year, I've continued to lose body fat, increased energy and improved fitness -- mental as well as physical.

Also... can't suppress the emerging sense of . . .
--Agelessness
--Invincibility
--Mental vigor

Travelling on this road too long...
No more stress now -- I'm straight
Now I get it now, I take time to think
Before I make a mistake
Just for my family's sake
That part of me left yesterday
The harder me is strong today
No regrets I'm blessed to say
The old me is dead and gone away

T.I. featuring Justin Timberlake
DEAD AND GONE

Courtesy of Youtube.com

The TrackYourPlaque program embodies fully the tools to engage comprehensively in the path toward infinite good health and reversal of many disease states -- diabetes, heart disease, peripheral vascular disease, erectile dysfunction, carotid artery disease, strokes, hypertension, obesity, hypothyroidism.

We're launching TYP 2.0 shortly in the next week or two. You'll truly be able to TRACK the wonderful progress in CAC score, lesion/volume/score, weight, BMI, Body Fat %, Lp(a), TC-TG-HDL-LDL, TSH, free T4, free T3, anti-TPO, CRP, fibrinogen, homocysteine, uric acid, creatinine, ALT, HDL2b, large small HDL, large small LDL, VLDL, IDL, etc. Supplement dose and durations can be entered eventually and tracked as well. These are the ULTIMATE tools for evaluating health and assessing improvements and trends.

I can hardly wait...

The next generation of TYP will be so exciting!!! I'm so glad y'll be there...

Currently we add our personal data HERE and soon will be greatly expanded.

Bliss out... let me kick it to ya! Grasp it!

Monday, July 14, 2008

TYPs: Success To Regress

Sometimes it does not hurt to hear the fundamentals repeated because we can be bogged down by advanced discussions on treatment, sophisticated lab testing or diagnostics.


Boiled down Track-Your-Plaque tips for success:

1. BMI -- achieve normal BMI. Advantages -- loss of toxic belly fat and increased metabolism. May take 3-6mos depending on degree of toxic belly fat.

2. Vitamin D3 -- obtain blood 25(OH)D to 60-70 ng/ml -- and Vitamin B3 Niacin (Slo-Niacin or NIASPAN) to raise HDLs. Clinical event reduction and plaque regression with these 2 powerful 'vitamins' cannot be overemphasized. The importance of raising HDL is reviewed here: TYP HDL Report. And we reviewed already here (at the end of the post).

3. Eliminate wheat, cornstarch and grains; Paleo diet RULES

4. Exercise/play/move -- increases metabolism, reduces inflammation, reduces mental stress, and prevents diastolic heart failure -- very common in people with NASH/NALFD and insulin resistance (like Metabolic Syndrome) and Type 2 Diabetes.

5. Do you exhibit elevated Lp(a) (or ultra low HDL)? If so, consider ultra high dose fish oil 8.5 g EPA+DHA daily (studies show only works when combined with moderate exercise/weight loss). Use high potency caps or liquid.

6. Strength training + Intermittent Fasting -- accelerates loss of toxic belly fat.
(However, if you have diabetic retinopathy, please avoid and discuss with your doctor. Extra cerebral pressures (like straining, Valsava, heavy weight lifting) can increase risk of retinal tears and subsequent vision changes/loss.)

7. For the first 1-2yrs of the TYP program, consider L-arginine. Benefits incl increasing NO in the vasculature which lower BP (goal (WSJ Joe Morgenstern's movie review 7/11/2008)? Do you need a trainer? As Wesley bluntly puts it at the end...after his 6 week-long life transformation toward purposeful, elite living... 'so wtf have you done lately...?'

-BG

Monday, June 23, 2008

Control Insulin (Part Two)

Briefly, the history of insulin and its relationship to atherosclerosis:

Stout RW. Insulin and atheroma. 20-yr perspective. Diabetes Care. 1990 Jun;13(6):631-54. Review. PMID: 2192848 Department of Geriatric Medicine, Queen's University of Belfast, Northern Ireland.
Many clinical studies have shown an increased insulin response to oral glucose in patients with ischemia of the heart, lower limbs, or brain. Hyperinsulinemia also occurs in patients with angiographically proved atherosclerosis without ischemia and thus appears to be related to arterial disease and not to be a nonspecific response to tissue injury. Fasting insulin levels and insulin responses to intravenous stimuli, including glucose, tolbutamide, and arginine, are normal, suggesting a gastrointestinal factor may be involved in the increased insulin response to oral glucose. In patients with atherosclerosis, insulin sensitivity appears to be normal or enhanced with respect to both glucose and lipid metabolism. Five population studies have shown that insulin responses to glucose are higher in populations at greater risk of cardiovascular disease. Many of the hyperinsulinemic populations also had upper-body obesity, hypertriglyceridemia, lower high-density lipoprotein (HDL) levels, and hypertension. These prospective studies support an independent association between hyperinsulinemia and ischemic heart disease, although their results differ in detail. Hyperinsulinemia is associated with raised triglyceride and decreased HDL cholesterol levels. Total and low-density lipoprotein (LDL) cholesterol is less closely related to hyperinsulinemia. Upper-body adiposity is associated (in separate studies) with coronary heart disease, diabetes, hyperinsulinemia, and hypertriglyceridemia. Insulin and blood pressure are closely related in both normotensive and hypertensive people. Although obesity and diabetes are often found in hypertensive people, hyperinsulinemia also occurs in nonobese nondiabetic hypertensive people. Thus, hyperinsulinemia is closely associated with a cluster of cardiovascular risk factors, i.e., hypertriglyceridemia, low HDL levels, hypertension, hyperglycemia, and upper-body obesity. There is a possibility that insulin has a role in the sex differences in ischemic heart disease incidence and their absence in diabetes, but additional work is required for its clarification. Long-term treatment with insulin results in lipid-containing lesions and thickening of the arterial wall in experimental animals. Insulin also inhibits regression of diet-induced experimental atherosclerosis, and insulin deficiency inhibits the development of arterial lesions. Insulin stimulates lipid synthesis in arterial tissue; the effect of insulin is influenced by hemodynamic factors and may be localized to certain parts of the artery. In physiological concentrations, insulin stimulates proliferation and migration of cultured arterial smooth muscle cells but has no effort on endothelial cells cultured from large vessels. Insulin also stimulates cholesterol synthesis and LDL binding in both arterial smooth muscle cells and monocyte macrophages.


Despres JP et al showed in the below study how elevated fasting insulin blood levels was closely associated to the presence of ischemic heart disease. The higher the concentration of insulin, the greater the odds ratio. And additionally they found other factors compounded the risk of heart disease:
--High Triglyercides
--High Total/HDL ratio (in other words, low HDL)
--High Apolipoprotein B


Després JP, Lamarche B, Mauriège P, Cantin B, Dagenais GR, Moorjani S, Lupien PJ.Hyperinsulinemia as an independent risk factor for ischemic heart disease.N Engl J Med. 1996 Apr 11;334(15):952-7. PMID: 8596596


Figure. Odds Ratios for Ischemic Heart Disease according to Plasma Insulin and Triglyeride Concentrations, Total:HDL Cholesterol Ratios, and Apolipoprotein B Concentrations. Insulin was measured after subjects had fasted for 12 hours. The median TG concentration (150 mg/dl [1.7mmol/L]), total:HDL ratio (6.0), and apoplipoprotein B concentration (119 mg/dl) were used to define men with either low levels (below the 50th percentile) or high levels (at or above the 50th percentile) for these variables. The results of tests of multiplicative interactions did not reach signficance at the 0.05 level for any of the combinations. P values are for comparisons with the reference group, which was assigned an addos ratio of 1.0. To convert values for insulin to picomoles per liter, multiply by 6.


The researchers Lemarche et al have done a great deal of research examining 'non-traditional risk factors '(see Table 2) and also showed the same link between insulin and associated ischemic heart disease.
Lamarche B, Tchernof A, Mauriège P, Cantin B, Dagenais GR, Lupien PJ, Després JP. Fasting insulin and apolipoprotein B levels and low-density lipoprotein particle size as risk factors for ischemic heart disease. JAMA. 1998 Jun 24;279(24):1955-61. (Full PDF here) PMID: 9643858

In fact, their results uncovered the fact that the largest odds ratio between traditional (LDL, TG, HDL) and nontraditional (small dense LDL, apo B and fasting insulin) fell to the Hyperinsulinemia risk factor. So high fasting insulin correlated stronger with the presence of evidence of coronary artery disease than than LDL-cholesterol. Triglyericides (TGs) even associated to a higher degree than LDL-cholesterol. HHmmmm?

Why do we always call LDL the 'bad' cholesterol? It appears that TGs is a bad character, indeed it appears TGs are the worse cholesterol out of all the traditional risk factors! Dr. Davis has pursued a lower TG goal lower than 'traditional' guidelines for many years. Current 'conventional' cardiovascular advice aims for TGs less than 150 however the Track Your Plaque program advocates an aggressive TG goal of 'normal' less than 60.

Is the 'LDL-cholesterol hypothesis' completely bunk?

Shouldn't Triglyerides be known as the 'lousy/bad' cholesterol?

Is this why statin-monotherapy fail to prevent signficant mortality and morbidity caused by plaque in heart disease and strokes?

The TYP goals for regression of ischemic heart disease are 60-60-60-60 (TG-HDL-LDL-25(OH)D). Many achieve this and beyond -- HDLs 80-90s and TGs 25-50s in the program!

And Elevated Fasting Insulin goal is not just less than 12 mU/L as discussed in the 2nd study above but at TYP the goal for regression is normal fasting insulin levels less than 5-10 mU/mL (30-60 pmol/L).

Is this why the Track Your Plaque program controls plaque comprehensively and trumps all 'conventional' cardiology programs by controlling triglycerides and insulin by a multifaceted strategy?
--Vitamin D3
--Wheat and grain cessation
--Exercise
--Weight loss to achieve normal BMI
--High/ultra-high dose fish oil EPA+DHA
--Hormone optimization (estrogen, testosterone, DHEA, etc)
--Vitamins K2/E/A
--Et cetera



Conclusions by the above authors Lamarche, et al:
'Beyond the mechanisms underlying the atherogenicity of hyperinsulinemia, hyperapobetalipoproteinemia, and small, dense LDL, and irrespective of whether these mechanisms share common paths, results of the present study suggest that the risk of IHD is increased substantially when these metabolic abnormalities cluster. The synergistic contribution of the nontraditional cluster of risk factors to IHD risk and the fact that almost 1 of every 2 IHD cases had these abnormalities simultaneously reflect the multifactorial etiology of IHD. It also emphasizes the importance of defining the risk of IHD based on more than 1 risk factor.
There are a number of critical issues that have to be considered before any decision can be made toward the measurement of these nontraditional risk factors on a routine basis. Among others, results of this prospective case-control study will have to be confirmed through larger population-based studies, as the relatively low number of IHD cases allowed only a gross assessment of risk. The relatively large CIs associated with the estimated risk in some of the subgroups reflect this phenomenon. Population reference values such as those used for LDL-C, triglycerides, and HDL-C also will be needed before critical levels of fasting insulin, apolipoprotein B levels, and LDL particle size or density at which a person becomes at greater risk for IHD are identified. Means to achieve effective treatment of the nontraditional risk factors is also a critical issue that deserves a great deal of scrutiny before decisions can be made toward use of these variables in the risk management of IHD. There are data to suggest that LDL particle size can be modulated by changes in plasma triglyceride levels.
41 Studies have shown that triglyceride-lowering therapy with fibric acid derivatives can lead to a significant increase in LDL particle size.42-43 There is also a large body of evidence demonstrating that LDL particle size, apolipoprotein B level, and insulin resistance and/or hyperinsulinemia can be effectively altered by diet and exercise-induced weight loss.44-45 Thus, the ability to favorably modify the nontraditional risk factors by diet, exercise, and appropriate pharmacotherapy provides further support for the use of these risk factors in the management of IHD risk...'



Lawlor DA, Fraser A, Ebrahim S, Smith GD. Independent associations of fasting insulin, glucose, and glycated haemoglobin with stroke and coronary heart disease in older women. PLoS Med. 2007 Aug;4(8):e263. PMID: 17760500
Full PDF here:

Editor's Summary
Background: Narrowing of the vessels that take blood to the heart and brain is a common form of cardiovascular disease—i.e., a disorder of the heart and blood vessels. It is a major cause of illness and death. By starving the heart and brain of oxygen, this condition causes coronary heart disease (CHD; heart problems such as angina and heart attacks) and strokes. A major risk factor for CHD and strokes is diabetes, a common chronic disease characterized by high levels of sugar (glucose) in the blood. In people who don't have diabetes, the hormone insulin controls blood-sugar levels. Insulin, which is released by the pancreas after eating, “instructs” insulin-responsive muscle and fat cells to absorb the glucose (released from food) from the bloodstream. In the very early stages of type 2 diabetes (the commonest type of diabetes, also called “adult onset” or “noninsulin-dependent” diabetes”), muscle and fat cells become unresponsive to insulin, so blood-sugar levels increase. This is called “insulin resistance.” The pancreas responds by making more insulin. As a result, people with insulin resistance have high blood levels of both insulin (hyperinsulinemia) and glucose (hyperglycemia). Eventually, the insulin-producing cells in the pancreas start to malfunction, insulin secretion decreases, and type 2 diabetes is the result.
Conclusions:
'Our findings indicate that amongst older women without diabetes and with fasting glucose levels in the normal range, fasting insulin is a stronger predictor of CHD and stroke risk than are fasting glucose or HbA1c.'
In addition, the results demonstrated a 'positive linear association between fasting insulin and CHD and stroke events is consistent with findings from the Atherosclerosis Risk in Communities study (SEE LAST CITATION), in which there was a positive linear association with CHD events that remained after adjustment for other CHD risk factors amongst women, but not amongst men [27]. A metaregression analysis of 17 prospective studies, primarily conducted in men and younger age groups than the current study, found a pooled relative risk of CHD per 50 pmol/l of insulin of 1.18 (95% CI 1.08–1.29) [9], which is consistent with our fully adjusted association with CHD (our results equate to 1.13 [95% CI 1.01–1.27] per 50 pmol/l of insulin). Overall the evidence suggests a modest positive association between fasting insulin and CHD events in women and men. Fasting insulin may exert its effect on cardiovascular risk via a direct impact on endothelial function [28,29].'



CRACK DOWN on insulin... CRACK DOWN on plaque (and cancer)...

Hunger will disappear away as well. Part of insulin's purpose is to drive energy into cells for storage. Insulin drives hunger as well. (...and mainly the consumption of carbs drive insulin secretion)
You will realize the benefits of low blood insulin and will often 'forget' to eat without prompting from this powerful hormone. You'll hunger for other things... vitality, movement, effortless-boundless ENERGY.


Importance of controlling triglycerides and insulin:

INSULIN ==> TG/HDL ratio ==> SMALL DENSE LDL

Zavaroni I, Dall'Aglio E, Alpi O, Bruschi F, Bonora E, Pezzarossa A, Butturini U.
Evidence for an independent relationship between plasma insulin and concentration of high density lipoprotein cholesterol and triglyceride.
Atherosclerosis. 1985 Jun;55(3):259-66.
PMID: 3893447 [PubMed - indexed for MEDLINE]

Ghiselli G, Bon GB, Soldan S, Avogaro P.
Regulatory function of glucose and insulin on high-density lipoprotein cholesterol in normolipidemic subjects.
Metabolism. 1994 Nov;43(11):1332-7.
PMID: 7968586 [PubMed - indexed for MEDLINE]

Cominacini L, Garbin U, Davoli A, Campagnola M, De Santis A, Pasini C, Pastorino AM, Bosello O.
High-density lipoprotein cholesterol concentrations and postheparin hepatic and lipoprotein lipases in obesity: relationships with plasma insulin levels.
Ann Nutr Metab. 1993;37(4):175-84.
PMID: 8215234 [PubMed - indexed for MEDLINE]

Laws A, King AC, Haskell WL, Reaven GM.
Relation of fasting plasma insulin concentration to high density lipoprotein cholesterol and triglyceride concentrations in men.
Arterioscler Thromb. 1991 Nov-Dec;11(6):1636-42.
PMID: 1931867 [PubMed - indexed for MEDLINE]

Stalder M, Pometta D, Suenram A.
Relationship between plasma insulin levels and high density lipoprotein cholesterol levels in healthy men.
Diabetologia. 1981 Dec;21(6):544-8.
PMID: 7040144 [PubMed - indexed for MEDLINE]

Tchernof A, Lamarche B, Prud'Homme D, Nadeau A, Moorjani S, Labrie F, Lupien PJ, Després JP.
The dense LDL phenotype. Association with plasma lipoprotein levels, visceral obesity, and hyperinsulinemia in men.
Diabetes Care. 1996 Jun;19(6):629-37.
PMID: 8725863 [PubMed - indexed for MEDLINE]

Laws A, Reaven GM.
Evidence for an independent relationship between insulin resistance and fasting plasma HDL-cholesterol, triglyceride and insulin concentrations.
J Intern Med. 1992 Jan;231(1):25-30.
PMID: 1732395

Katzel LI, Coon PJ, Rogus E, Krauss RM, Goldberg AP.
Persistence of low HDL-C levels after weight reduction in older men with small LDL particles.
Arterioscler Thromb Vasc Biol. 1995 Mar;15(3):299-305.
PMID: 7749838

McNamara JR, Jenner JL, Li Z, Wilson PW, Schaefer EJ. ***
Change in LDL particle size is associated with change in plasma triglyceride concentration.
Arterioscler Thromb. 1992 Nov;12(11):1284-90.
PMID: 1420088

Folsom AR, Szklo M, Stevens J, Liao F, Smith R, Eckfeldt JH. **
A prospective study of coronary heart disease in relation to fasting insulin, glucose, and diabetes. The Atherosclerosis Risk in Communities (ARIC) Study.
Diabetes Care. 1997 Jun;20(6):935-42.
PMID: 9167103


-G

Sunday, June 15, 2008

'Wanted': Elite Heart Health NOW

There is a new summer blockbuster I'm looking forward to...(!!) 'Wanted' shortly will be released. Angelina Jolie plays a sort of 'trainer'... to a novice apprentice. All the tools to assassinate the target are provided, and he is 'invited' to lead a new life. Do we all have opportunities to transcend and create extraordinary goals? ...And achieve what we never dreamed? Would you know unless the first steps are taken? Do you need a trainer?

Shift time... Shift your destiny... and make every minute count.

Live like you mean it

Don't accept a 'normal' standard heart life (ie, 'conventional cardiovascular care')
Don't expect mediocrity
Don't wait for an AED defibrillator to be mandated for each home for a home myocardial infarction
Don't play with fire...

Protect a life, yours, and protect others, those who depend on you

Learn all the weapons to l-i-v-e... super-vital, plaque-free, extra-extended lives

Forge elite heart health and fitness now


'This is your destiny. Join us...' Morgan Freeman


Choose your destiny

Choose elite heart health now...And change your life forever...

Track Your Plaque (TYP 2.0):
--controls plaque
--controls weight and body fat
--controls TGs ('bad cholesterol') and small dense bullet-like LDL
--controls blood pressure
--controls inflammation and insulin
--controls glucoses
--controls heart rhythms
(These interventions also controls the same factors which cause strokes, ED, and most cancers.)

Do you need a trainer?

-G

Saturday, May 24, 2008

Plaque, Plaque, and... More Plaque Reversal

"Remodelling of alveolar bone involves interaction between osteoblasts and osteoclasts. Osteoblasts, under the influence of osteotropic hormones (vitamin D3, PTH and retinoic acid), produce MMPs which appear to function in the removal of soft tissue that precludes access of osteoclasts to the mineralized tissue surface.... Although there is strong evidence for the involvement of MMPs in the resorption of bone and in the inflammation-mediated destruction of periodontal tissues, the role of MMPs in the remodelling of mature soft connective tissues remains equivocal."

Sodek J, Overall CM. Matrix metalloproteinases in periodontal tissue remodelling. Matrix Suppl. 1992;1:352-62. Review. PMID: 1480060


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Boyd LD, Lampi KJ. Importance of nutrition for optimum health of the periodontium. J Contemp Dent Pract. 2001 May 15;2(2):36-45. Review. PMID: 12167932 Link HERE *good review*


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Figure. Activation mechanisms of MMP-2. The full-length MMP-2 can be activated in two ways. Proteolytic activation of MMP-2 by MT1-MMP/TIMP or by other proteases occurs by removal of the autoinhibitory propeptide domain (left arrow) resulting in an active truncated MMP-2. The presence of oxidative stress (ONOO-) and cellular glutathione (GSH) causes the S-gluathiolation of the critical cysteine residue in the propeptide domain, disrupting its binding to the catalytic Zn2+ ion, resulting in an active full-length enzyme. MMP, matrix metalloproteinase; ONOO-, peroxynitrite; TIMP, tissue inhibitor of metalloproteinase. Chow AK, et al. Acute actions and novel targets of matrix metalloproteinases in the heart and vasculature. Br J Pharmacol. 2007 Sep;152(2):189-205.


Recently we moved and lost our housekeepers. I've been in the double-dog dumps ever since... So to say the cleaning of the house has been neglected is a very grave understatement. Last week I devoted an inordinate amount of time scouring the calcium deposits off all the toilets in the house... it took so long so I had a long time to think. Why (??!) did I wait so long? Why did I let this thing go?? The work was so much harder and and tougher than had I just kept up with routine maintenance weekly. Right? (Also have spent time weighing the benefits of hiring professionals again) My girlfriends love using CLR (above ad) but I hesitate using such a strong cleaning solvent on the toilets not just for the environmental impact but also the corrosive effects on the pipes (not withstanding other effects such as melting my corneas and the first 2 layers of my skin -- rubber gloves are mandatory).

As I was really getting into the scrubbing and facing the challenge of getting back an immaculate white and tidy bowl, I thought is this what my nazi-Dental Hygienist thinks every time she sees me as she sharpens her metal instruments for scraping tartar and plaque off the teeth? A few years ago I was diagnosed with gum disease with pockets of '4' and '5' and told that implants and antibiotic treatment et cetera might be required some day. When you have periodontal disease, extra cleanings (btw are NOT covered by insurance) and deep scaling/root planing (yes it's as nasty as it sounds) are required to control plaque with the hopes of reducing inflammation and further damage. Gum disease actually involves similar processes that atherosclerosis/heart disease involves, including destruction by excessive MMPs. On the surface of atherosclerotic plaques in our blood vessels, MMPs are found. Destabilization of plaque has been related to overactivity of MMPs. The above article demonstrates the value of vitamin D3 and vitamin A (retinoic acid) and PTH in ameliorating gum disease and correcting the balance between building (osteoblastic activity) and cutting (osteoclastic activity) of our mature gum soft tissues. Interestingly these agents, Vitamins D3 and A, also have incredible plaque-busting benefits in the Track Your Plaque program for CAD regression and eradication. Dr. Davis demonstrated the value of Vitamin D3 in shrinking plaque in coronary arterties and heart disease reversal.


My gum disease now has reversed. I've attributed all the benefits to a low-inflammatory diet (ie rich in good oils, protein, veggies and low low carb), exercise, A-N-D vitamins D3, A and high dose EPA + DHA fish oil. At the end of sumer last year, surprisingly, my lab 25(OH)D3 was extremely low (after being in the sun daily for hours with the kids at the pool). Correction of vitamin D deficiency was one component of improving periodontal disease (obtaining blood levels of 50-60 ng/ml). Happily, at my last visit to the dentist, my gums were given a clean bill of health. Nearly all the pockets were '3's and a few '4's now. The '5's had disappeared and I was told I could return to a normal bi-annual cleaning schedule again (and no more out-of-pocket cleanings). The throbbing that I once felt in the gums are gone too.

Other MMP inhibitors include Doxycline (part of the tetracycline family of drugs). It is a prescription drug which is used in the treatment of periodontal disease and gingival inflammation but has also demonstrated some value in atherosclerosis and preventing heart failure remodeling. PERIOSTAT is a brandname Doxycline indicated by the FDA for treatment of gum disease.
  • Tessone A, et al. Effect of matrix metalloproteinase inhibition by doxycycline on myocardial healing and remodeling after myocardial infarction. Cardiovasc Drugs Ther. 2005 Dec;19(6):383-90. PMID: 16435072
  • Chow AK, Cena J, Schulz R. Acute actions and novel targets of matrix metalloproteinases in the heart and vasculature. (see above Figure) Br J Pharmacol. 2007 Sep;152(2):189-205. Epub 2007 Jun 25. Review. PMID: 17592511


    I wish I could stick vitamin D in all my toilets everyday... *heh*
  • Dietrich T, et al. Association between serum concentrations of 25-hydroxyvitamin D and gingival inflammation. Am J Clin Nutr. 2005 Sep;82(3):575-80. PMID: 16155270

    Rickets -- a profound vitamin D deficiency condition which frequently involves signficant dental disease (because vitamin D plays a vital role in calcification of teeth and remodeling of soft gum tissues).
  • Chaussain-Miller C, et al. Dentin structure in familial hypophosphatemic rickets: benefits of vitamin D and phosphate treatment. Oral Dis. 2007 Sep;13(5):482-9. PMID: 17714351
  • Yamamoto T. Diagnosis of X-linked hypophosphatemic vitamin D resistant rickets.
    Acta Paediatr Jpn. 1997 Aug;39(4):499-502. Review. PMID: 9316300
  • Chaussain-Miller C, et al. Dental abnormalities in patients with familial hypophosphatemic vitamin D-resistant rickets: revention by early treatment with 1-hydroxyvitamin D. J Pediatr. 2003 Mar;142(3):324-31. PMID: 12640383

    Dental insurances allow one extra covered dental cleaning during pregnancy. Studies show that the pregnancy-state increases the risk of periodontal disease (likely secondary to cortisol, inflammation, insulin? vitamin D and EPA/DHA deficiency? I would presume). Prevention with an extra cleaning is therefore now advocated. Isn't that interesting? Pregnancy may significantly deplete vitamin D stores (unless replenished) -- in order to construct enough progesterone and estrogen which are also steroidal hormones for supporting the pregnant state. Both pregnancy and lactation also reduce the mother's stores of EPA+DHA in her brain and heart in order to supply the growing fetus/baby's brain and heart. Did you know that a baby's brain is 70% of its birth weight? And did you know that breastmilk is a rich source of 'fish oil' EPA + DHA !

    This researcher believes that maternal imprinting can affect CAD risk later in life. By not consuming enough good oils during conception and pregnancy, are we affecting our children later in life? He strongly believes fish oil may protect and even prevent CAD and diabetes in children when maternal EPA and DHA are adequately provided.
  • Das UN. A perinatal strategy to prevent coronary heart disease. Nutrition. 2003 Nov-Dec;19(11-12):1022-7. Review. PMID: 14624957

  • Cerná H, et al. Acta Univ Palacki Olomuc Fac Med. 1990;125:173-9. Periodontium and vitamin E and A in pregnancy.
    The evaluation of the clinical condition of periodontium by means of the epidemiological indexes and the level of oral hygiene in two weeks intervals in the course of physiological pregnancy in 39 women in good general health revealed the maximum of inflammatory changes of periodontium in the 8th month of pregnancy with the amelioration shortly before delivery. Simultaneous follow-up of the physiological levels of vitamin E and A in four weeks intervals showed the decline of the mean levels of both vitamins in the course of the 8th month and their marked elevation shortly before delivery; therefore remains questionable, if this elevation reaching over their physiological range, contributes to the amelioration of the condition of periodontium observed at the same time. PMID: 2150274

    Phenytoin is a drug that increases the liver metabolism of certain drugs and hormones, including Vitamin D and Vitamin A. Seizure and other individuals taking Phenytoin can be at risk not only for osteoporosis but also gum disease (and heart disease and many over conditions) due to subsequently low vitamin D levels. (Isotretinoin is a synthetic vitamin A)
  • Norris JF, Cunliffe WJ. Phenytoin-induced gum hypertrophy improved by isotretinoin. Int J Dermatol. 1987 Nov;26(9):602-3. No abstract available. PMID: 2965113
  • Lucchesi JA, et al. Severe phenytoin-induced gingival enlargement associated with periodontitis. Gen Dent. 2008 Mar-Apr;56(2):199-203; quiz 204-5, 224. PMID: 18348382
  • Hall EE. Prevention and treatment considerations in patients with drug-induced gingival enlargement. Curr Opin Periodontol. 1997;4:59-63. Review. PMID: 9655022
  • Sobaniec H, et al. Antioxidant activity of blood serum and saliva in patients with periodontal disease treated due to epilepsy. Adv Med Sci. 2007;52 Suppl 1:204-6. PMID: 18229666


    Vitamin A is also helpful for reversing gum disease in a condition called Papilon-Lefevre syndrome.
  • Nazzaro V, et al. Papillon-Lefèvre syndrome. Ultrastructural study and successful treatment with acitretin. Arch Dermatol. 1988 Apr;124(4):533-9. PMID: 2965550

    When I think about inflammation and the crucial role fish oil plays in maintaining healthy hearts and minds.... I am not shocked to find out it also regulates healthy gums and oral health. Friends on the TYP forum on the other hand will be shocked that I've reduced my dose of fish oil (slightly) since our family started drinking grass-raised cow milk which is rich in EPA+DHA, CLA, vitamins A D3 E and K2. I love fish oil for all its amazing benefits. Here is more evidence for its healing properties on gingival inflammation (and the hypothesized relationship with vascular inflammation).
  • Fish oil reduces tooth loss mainly through its anti-inflammatory effects?
    Hamazaki K, et al. Med Hypotheses. 2006;67(4):868-70.
    Competing at several steps of arachidonic acid metabolism, n-3 fatty acids reduce production of highly active prostaglandins and leukotrienes and exert anti-inflammatory effects. They are also experimentally shown to be anti-osteoporotic. Periodontitis is responsible for most tooth loss in adult populations. If enough n-3 fatty acids are provided, periodontitis with alveolar bone resorption may be controlled, and tooth loss may be prevented. In fact, n-3 fatty acid administration lowered prostaglandin E(2) production, tooth movement and alveolar bone resorption in animal experiments. Aggression, which may be related with tooth loss, was also controlled with fish oil. Our cross-sectional data supported our hypothesis. We recruited 256 men (22-59 y of age) and 95 women (22-66 y), counted the numbers of their remaining teeth, and analyzed the fatty acid composition of the total phospholipid fraction of RBCs. The beta-coefficient of the numbers of remaining teeth and EPA concentrations in the fraction was 0.89 (per 1% EPA, p=0.007) after adjustment for 9 possible confounding factors. Long-term intervention studies with fish oil planned in the future should be able to test our hypothesis by just adding another very simple endpoint in those studies: tooth loss during the intervention period. This hypothesis may explain the linkage between periodontitis/tooth loss and coronary heart disease. PMID: 16759817

  • Campan P, et al. [Polyunsaturated omega-3 fatty acids in the treatment of experimental human gingivitis] Bull Group Int Rech Sci Stomatol Odontol. 1996 Feb-Mar;39(1-2):25-31. French. PMID: 8720373
  • Kesavalu L, et al. Omega-3 fatty acid effect on alveolar bone loss in rats. J Dent Res. 2006 Jul;85(7):648-52. PMID: 16798867
  • Kesavalu L, et al. Omega-3 fatty acid regulates inflammatory cytokine/mediator messenger RNA expression in Porphyromonas gingivalis-induced experimental periodontal disease. Oral Microbiol Immunol. 2007 Aug;22(4):232-9. PMID: 17600534
  • Requirand P, et al. Serum fatty acid imbalance in bone loss: example with periodontal disease. Clin Nutr. 2000 Aug;19(4):271-6. PMID: 10952799
  • Iwami-Morimoto Y, Yamaguchi K, Tanne K. Influence of dietary n-3 polyunsaturated fatty acid on experimental tooth movement in rats. Angle Orthod. 1999 Aug;69(4):365-71. PMID: 10456605


    Nutritional factors play the same important roles in parallel organs in our body. Perhaps proper vitamins/food and fish oil everyday will not only keep the doctor away...

    But also my nazi-hygienist! :)

    If only the same were true for all other types of housekeeping.

    (Thanks go out to Mr.California for his super-RICH ideas. You deserve an 'S' emblazoned on your chest for sharing your fascinating cardiovascular-related thoughts and insights.)

  • Friday, March 21, 2008

    Immortality, Vampires and T-Y-P

    Want to live forever?
    (End of video NSFW)

    (San Francisco, Godfather-like, feuding vampire
    clans, compelling characters; only o-n-e season??
    Courtesy of Youtube.com)

    During the '90s I enjoyed many shows and movies w/a similar theme... Remember these?

    I'm an immortality-groupie... (that's why I'm here)

    What are the characteristics of immortality?

    --Hotness (although not required)-- (have you ever heard of a vampire with wheat-belly? of course, absolutely sunlight-resistance...)
    --Zen-quality calm and fearless focus
    --Absence of plaque or vascular disease or erectile dysfunction (future blog topic)
    --Live forever (this is a sorta requirement)

    You don't have to be bitten by a vampire to live supernaturally long... like Mr. Nicholas de Brabant of the moralistic series Forever Knight (see below). He was the reluctant vampire who preferred to drink from lab samples in his girlfriend's pathology fridge.
    There are many things that elongate telomeres, and therefore lengthen lifespan and induce unsurpassable mortality.

    Telomeres are the caps at the end of nuclear DNA (chromosomes), like a strand of pearls on a necklace. The longer the strand, the longer the life of the organism and cells.

    Want to experience maximal lifespan extension?
    Vitamin D may be your link to immortality (like a vampire -- without all the biting and body bags) through the TrackYourPlaque program.

    A few years ago, this discovery was made by Dr. Davis (even prior to the telomere connections) in Wisconsin. How in the world did Dr. 'D' aspire to such a cure? Why is he so divine? Divine... like Da Vinci... Someone even compared his prescient abilities in eludicating tools to eradicate plaque to the 'Nostradamus of heart disease'.. or 'even doggone spooky'... like... X-files Fox Mulder...!

    Dr. D is truly an extraordinary cardiothoracic-surgeon... doing extraordinary things.

    FOREVER KNIGHT
    (Once in a Lifetime by Sisters of Oz)
    (Courtesy of Youtube.com)

    OVERVIEW:

    Cardiovascular risk modulators and telomere length reducers:
    • Vitamin D deficiency (25(OH)D less than 50 ng/ml)
    • Oxidative stress
    • Psychological stress (ie, sleep deprivation)
    • Hypertension
    • Estrogen deficiency
    • Sedentary during leisure time
    • Insulin resistance (ie, NAFLD, cardiac steatosis, metabolic syndrome, PCOS)
    • Type 2 Diabetes
    • Type 1 Diabetes
    • Obesity
    • Homocysteine
    • Smoking
      (All of the above are modifieable factors in the TrackYourPlaque program)

    Fuster JJ, Andrés V. Circ Res. 2006 Nov 24;99(11):1167-80. Telomere biology and cardiovascular disease.
    Richards JB, Valdes AM, Gardner JP, Paximadas D, Kimura M, Nessa A, Lu X, Surdulescu GL, Swaminathan R, Spector TD, Aviv A. Higher serum vitamin D concentrations are associated with longer leukocyte telomere length in women. Am J Clin Nutr. 2007 Nov;86(5):1420-5.
    Aviv A.
    Hypothesis: pulse pressure and human longevity. Hypertension. 2001 Apr;37(4):1060-6.
    W. Browner, et al.
    The genetics of human longevity. The American Journal of Medicine, Volume 117, Issue 11, Pages 851-860.
    Kenyon C. The plasticity of aging: insights from long-lived mutants. Cell. 2005 Feb 25;120(4):449-60.
    Njajou OT, Cawthon RM, Damcott CM, Wu SH, Ott S, Garant MJ, Blackburn EH, Mitchell BD, Shuldiner AR, Hsueh WC.
    Telomere length is paternally inherited and is associated with parental lifespan. Proc Natl Acad Sci U S A. 2007 Jul 17;104(29):12135-9.
    Haussmann MF, Mauck RA. Telomeres and longevity: testing an evolutionary hypothesis. Mol Biol Evol. 2008 Jan;25(1):220-8.
    Richards JB, et al. Homocysteine levels and leukocyte telomere length. Atherosclerosis. 2008 Feb 14; [Epub ahead of print]
    Cherkas LF, et al. The association between physical activity in leisure time and leukocyte telomere length. Arch Intern Med. 2008 Jan 28;168(2):154-8.

    (i've got infinite un-perpetual links, sorry in advance!)

    Sunday, March 9, 2008

    Homage to the American Heart Association

    This is homage to the AHA... love you guys...

    Today... But it may change TOMORROW...

    February, the American Heart Health Month has passed...

    Is there hope offered beyond low fat, insulinogenic diabetes-generating diets, statins, interventionalist surgeries and stents by the common cardiovascular community?

    Why still is vascular disease the #1 killer of men and(increasingly) women?

    The hope for the future is that plaque eradication is here already...

    One thing that the AHA has progressively portrayed is their Advocacy for Cure campaign: 'You are the CURE'.

    And the second things is that the AHA supports: heart scans.

    Work collaboratively with your team including physician/cardiologist/NP/PA/PT/ NURSE/pharmacist/personal trainer/chef/etc and get empowered with the T-Y-P program.

    And advocate your own C-U-R-E . . .


    (at her Dublin Ireland concert, Avril dedicates this particular song to her grandfather who slipped away earlier that day, from what I believe was without warning vascular disease (stroke); I didn't post her tearful performance b/c it's painful to watch)



    Couldn't have said it any better...



    TOMORROW

    By Avril Lavigne


    And I wanna believe you
    When you tell me that it'll be ok
    Ya... I try to believe you

    B-U-T . . . I D-O-N- 'T . . .
    When you say that it's gonna be
    It always turns out to be a different way
    I try to believe you

    NOT T-O-D-A-Y , today, today, today, today...

    [Chorus:]I don't know how I feel
    tomorrow, tomorrow
    I don't know what to say
    tomorrow, tomorrow
    Is a different day
    It's always been up to you
    It's turning around
    IT'S UP TO M-E

    [remember... YOU ARE THE CURE, according to the AHA]
    I'm gonna do what I have to do
    Just don't give me a little time
    Leave me alone a little while
    Maybe it's not too late
    Not today, today, today, today, today...

    I'm not ready
    Maybe tomorrow
    And I wanna believe you
    When you tell me that it'll be ok
    Ya I try to believe you
    Not today, today, today, today, today... Tomorrow it may change

    Wednesday, March 5, 2008

    Seeing is not believing

    I met a friend in college named Rick (well, of course, not real name but close enough). He was the son of a wealthy soda-pop executive and looked like a blond godversion of Richard Gere (same swagger pre-Buddhism days.)

    Since childhood, Rick had an optic nerve disorder that left his vision narrowed to a field within only 2-4 inches of his eyes. His wicked sense of humor was intense and empathy even more exquisite. He could tell our mood by just a few cues like voice or posture. His articulation of life was indescribable.
    Rick wasn't born with amazing senses of smell, taste, touch or hearing (or drinking with his frat mates). These were honed skills (like imbibing). It seemed with a disruption of the one single visual sense, the other routes of his perception of the world were super-trained. Super-heightened. SUPER-freightening. Way above and way beyond normal.

    When someone engages in a TYP-styled life and adjunct therapy, similarly, multiple pathways for plaque-regression are super-charged, super-optimized. Plaque growth immediately halted. Plaque damage overridden... eventually eradicated. Anginal pains go away. We all have the ability to be whole and complete. Our bodies hold the key to these resources and the capacity to heal. Don't believe?

    Read about the TYP successes. Many people share achievements on the forum with (mild) pride--it's not necessarily an easy task. Incredible outcomes happen all the time. Although small dense atherogenic LDL numbers are reduced in nearly all cases, the most reliable index for plaque eradication is demonstrated when EBT scan measurement (scored at baseline then infrequent intervals) reductions occur to 10%, 20% or even record-breaking 50-60% levels. Seeing how healthy one lives or wonderful lab measurements are not necessarily adequate. Looking hot, hip and healthy aren't enough for heart and vascular disease prevention. As even my mechanic could tell you, relying on sight offers no guarantees, (and this is why he charges me a lot for running diagnostic tests). Even the most energetic marathoner can have silent indicators of heart disease and isn't aware. Just like lumps and bumps (polyps), asymptomatic plaque is hidden -- undetectable to the naked eye.

    Scans are not done often (routinely, in similar fashion to cancer preventive screening tools, i.e. mammograms or sigmoids). Yet these are the only tools and metrics that conveniently, safely and quickly assess the presence of plaque (also, inexpensively, with minimal radiation, and without dyes that harm kidneys).

    What does scanning offer? Not much but a number (and a pretty picture). That number (positive calcium score) is irrefutable and pathognomic for plaque. It's like a financial debt or a crazy lover -- don't want one, to be undone, right?

    Europeans are perhaps more advanced than the U. S. for using heart scan screenings to reduce unnecessary death, disability and damage from heart disease.

    Non-invasive screening for coronary artery disease: calcium scoring

    Cardiac computed tomography: indications, applications, limitations, and training requirements

    Determinants of Progression of Coronary Artery Calcification in Type 2 Diabetes: Role of Glycemic Control and Inflammatory Vascualr Calcification Markers


    Ok... let's give the U.S. some credit now! In addition to Dr. Davis, here is another luminary endorsement of scans for screening:
    Noninvasive Screening for Coronary Atherosclerosis and Silent Ischemia in Asymptomatic Type 2 Diabetic Patients, Dr. George A. Beller, MD, MACC, Cardiovascular Division, Virginia.

    And like Dr. Davis, a physician (in primary care, no less--say YAHHH for the primary care in the deep trenches) who experienced virtually no cardiovascular events in his primary care practice in Colorado (no CAD surgeries, no cabgs, no stents, no PTCAs, no MIs, no deaths):
    Dr. William Blanchet, MD

    If there is premature vascular disease in the family tree (stroke, heart disease or surgeries, ED, kidney disease, ocular strokes, aneurysms, etc), then do not be fooled. Risks are present even with the so-called healthiest living. Even if you are not blind like Rick, in regards to the vigor of the heart, know that seeing is not believing.