Abs 2 Die 4...FAQs

This summary is not available. Please click here to view the post.

Evoke Tranquility...

J. L. Merlin
Evocacion

Courtesy of Youtube.com

Melatonin has been on my mind...ever since Dr. D got me turned on to it here a little while ago. I know several people who take it and TOTALLY swear by it for insomnia. How can this hormone have such far-reaching benefits and effects?

It's used for:
--jet lag
--inducing hGH secretion
--hypertension
--breast cancer prevention
--oxidative damage protection
--insomnia
--vasculature un-responsiveness (relaxation/constriction with ACh or adrenaline)
--migraine prevention
--modulation of behavior and sleep patterns in autistic children
--natural aromatase inhibitor -- prevents excessive conversion of Testosterone to Estradiol (E2) and Androstenedione to Estrone (excessive Estrone (E1) is not good -- 'storage' form of estrogen in our adipose tissues and linked to promotion of cancer...and ??perhaps heart disease?)

Melatonin also is the master hormone behind skin changes in amphibians and reptiles.

How about us humans? You know how teenagers get all moody and starting staying up late and waking up late? And how they may transform from sweet kids to stinky Twilight sulkiness? Melatonin drops as sexual maturation occurs and this may lead to disrupted sleep cycles. This researcher and author of the textbook Dev Bio notes that Melatonin is the suspected hormone that allows human metamorphosis to occur: "The various morphological and behavioral changes of puberty are due to the actions of these hormones on the various target tissues. As in metamorphosis, there appears to be a maturation-inhibiting hormone whose activity decreases to permit the reactivation of development. In humans, this hormone is probably MELATONIN, whose serum concentration decreases as that of LH rises (Waldhauser and Dietzel, 1985)."


So who may experience dysregulation of Melatonin? Which came first...the chicken or the egg? Dysregulation of the hypothalamus/pituitary/pineal axis with wheat-assaults, in utero maternal vitamin D deficiency and/or neonatal/developmental EPA-DHA deficiency?

Are we epigenetically pushing our species into extinction?

The medical literature shows that many types of individuals are deficient in melatonin in the diurnal secretion that normally occurs at night -- in the pitch black inkiness of the night as nature intended (of course unless the full moon is shining). Normally melatonin starts to rise at 7pm and peaks at 2am then gradually falls again by dawn. Seasonal rhythms obviously exist also. Anciently controlled tides that we may not even be conscious of. In Scotland, scientists have recently shown how "Melatonin acts directly on anterior-pituitary cells, and these then relay the photoperiodic message back into the hypothalamus to control neuroendocrine output...(to trigger increases in TSH which subsequently signals activation of T3 (active thyroid hormone from T4) for increased metabolism and reproduction)...In mammals this provides the missing link between the pineal melatonin signal and thyroid-dependent seasonal biology (Hazlerigg Curr Biol. 2008 Aug 5;18(15):1147-52).

--Autistic spectrum children -- they tend to also display a genetic polymorphism, a deletion for the gene encoding the last enzyme for the making of Melatonin
--Individuals with coronary artery disease
--Type 2 diabetes with cardiac autonomic neuropathy (stiff heart rate variability (HRV))
--Wernicke-Korsakoff syndrome -- ie, brain-damage due to malnourishment -- seen in gastric bypass and alcoholics
--Sleep deprived individuals, swing shift workers, travel involving time zone shifts
--Hyperthyroid, hypothyroid (higher melatonin secretion but also higher elimination in the urine found)
--Environmental lighting conditions, drugs and other disease states: "Patients with alcoholism, migraine, postoperative pinealoma, panhypo-pituitarism, hereditary dystonia and schizophrenics on propranolol exhibited a decreased amplitude of their diurnal rhythm of melatonin." (Wetterberg L J Neural Transm Suppl. 1978;(13):289-310.)
--Fibromyalgia 31% less compared with healthy controls
--Alcohol consumption lowers Melatonin secretion 20% (HHHhhhmmmm...Patrone's+PEET*s apparently is a bad combo for my melatonin??? darn; don't worry -- light intake's fine)
--Obstructive sleep apnea







We are certainly learning a lot about the how all hormones are inter-related in the body. Like life, one disjointed connection can lead to impaired connections downstream. Are there ways to repair and strengthen the misconnected parts? I'm here at TYP...so I certainly believe in the plasticity of our bodies (and I aint referring to the wonders of silicon *wink*).

Thoughtful-mindfulness...meditation, prayer, yoga, tai-chi, massage, day-spa visits all achieve a level of control that is exerted on our 'third eye', the tiny pineal gland (see above; courtesy of here). I read a TIME magazine article ~2-3 yrs about how Buddhist monks were able to activate and light up parts of the brain on PET scans that normally are not associated with neural activity. They meditated (and according to the Dalai Lama teachings that I've read, this involves heightened awareness and enlightened empathy). Is this related to the Pineal Gland? Are there mechanisms that exist for synergizing our Pineal (found in the 3rd ventricle of the brain) with the rest of the brain, body and our deep unconsciousness? (like syncing an iPod to the computer?)

I dunno...but certainly other forms of meditation have been shown in small trials to result in significantly higher melatonin secretion from the Pineal Gland. Like a power nap an adequate night's slumber, how can plain old brain-power power up and protect our Pineal Gland? Apparently in very very very potent ways...! Maybe this justifies my addiction to day spas and yoga?

Tranquility is so super addictive.

Are we hard-wired for tranquility? Yes, I believe so once we are plugged into it.



Plaque-Busting Benefits of Yoga and Meditation
--"Experienced meditators practising either TM-Sidhi or another internationally well known form of yoga showed significantly higher plasma melatonin levels in the period immediately following meditation compared with the same period at the same time on a control night." (Sali A. Acute increases in night-time plasma melatonin levels following a period of meditation. Biol Psychol. 2000 May;53(1):69-78.)
--"Yogic practices for 3 months resulted in an improvement in cardiorespiratory performance (orthostatic tolerance, heart rate, BP, respiratory rate, dynamic lung function (such as forced vital capacity, forced expiratory volume in 1 second, forced expiratory volume percentage, peak expiratory flow rate, and maximum voluntary ventilation) and psychologic profile. The plasma melatonin also showed an increase after three months of yogic practices. The systolic BP, diastolic BP, mean arterial pressure, and orthostatic tolerance did not show any significant correlation with plasma melatonin. However, the maximum night time melatonin levels in yoga group showed a significant correlation (r = 0.71, p less than 0.05) with well-being score. Effects of Hatha yoga and Omkar meditation on cardiorespiratory performance, psychologic profile, and melatonin secretion. Sawhney RC J Altern Complement Med. 2004 Apr;10(2):261-8.)




Coronary/Vasculature Relationship and Role of Melatonin
Two publications from Northwestern med school recently reviewed the melatonin and the receptors that it binds and modulates: MT1, MT2, MT3. In one, the authors described the broad spectrum effects of Melatonin on a variety of organ systems (Masana MI Front Biosci. 2003 Sep 1;8:d1093-108. Molecular pharmacology, regulation and function of mammalian melatonin receptors). Like adrenaline (ie, NE/EPI) that binds beta- or alpha-receptors in various locations in our bodies, the end result can be inhibiting or stimulating activity; the physiological function depends on the location of the receptors as well. Likewise with Melatonin and the MT series, location and type of receptors determines function. Melatonin receptors affect every organ system: CNS (brain), hypothalamic-pituitary-pineal-thyroid-gonadal axis, cardiovascular, and immunity. The second article below describes inhibitory and activating effects of MT receptors.

Functional MT1 and MT2 melatonin receptors in mammals.
Dubocovich ML, Markowska M. Endocrine. 2005 Jul;27(2):101-10.

Melatonin, dubbed the hormone of darkness, is known to regulate a wide variety of physiological processes in mammals. This review describes well-defined functional responses mediated through activation of high-affinity MT1 and MT2 G protein-coupled receptors viewed as potential targets for drug discovery.

MT1 melatonin receptors modulate NEURONAL FIRING, ARTERIAL VASOCONSTRICTION, cell proliferation in cancer cells, and REPRODUCTIVE AND METABOLIC FUNCTIONS.

Activation of MT2 melatonin receptors phase shift circadian rhythms of neuronal firing in the suprachiasmatic nucleus, inhibit dopamine release in retina, INDUCE VASODILATION and inhibition of leukocyte rolling in arterial beds, and ENHANCE IMMUNE RESPONSES.

The melatonin-mediated responses elicited by activation of MT1 and MT2 native melatonin receptors are dependent on circadian time, duration and mode of exposure to endogenous or exogenous melatonin, and functional receptor sensitivity. Together, these studies underscore the importance of carefully linking each melatonin receptor type to specific functional responses in target tissues to facilitate the design and development of novel therapeutic agent. (OF COURSE! LET'S MAKE A PROFITABLE DRUG! ESP WHEN A CHEAP NATURAL ORIGINAL ALREADY EXISTS AND IS WIDELY AVAILABLE)
PMID: 16217123

And btw...STOP WHEAT
In polyglandular autoimmune thyroiditis (hypothyroidism), melatonin levels were naturally found to be low particularly when more fatigue was observed by the study participants. The more fatigue, additionally, the more auto-antibodies were found associated with more organs. The adrenals were attacked in addition to the ovaries, thyroid and/or TPO (thyroid peroxidase). It is not clear precisely the relationship between thyroid function, melatonin and auto-antibodies here... In trials looking at simple hypothyroidism, often melatonin levels are fine or mildly shifted. In the case where multiple glands/organs are affected, the melatonin effects appear more significant. I never realized we could make auto-antibodies to our adrenals. But the medical literature is chock full of stories of auto-antibodies produced against nearly ANYTHING in our bodies -- including our p450 enzymes and even...(!!) mitochondria (our little nuclear ATP powerhouses).

??Can we possibly produce auto-antibodies to our pineal? Or calcify it to rock or pebble? Why not? I believe we could...

Wheat as you aware is not only a common food allergen, but it increases gene expression (62 in this trial detected) of a variety of stress hormones, cytokine-chemokine–mediated immunity, and the interleukin pathway, and MMPs (metalloproteinases) (prior post on the FUNGENUT study). Does wheat trigger the increased production of auto-antibodies? Absolutely. Hypothyroidism is a common autoimmune manifestation of silent celiac disease, in other words wheat intolerance. Other organs or tissues frequently 'burnt to a toast' include: Fingers/Rheumatoid; Wrists/CTS; Knees/osteoarthritis; Gallbladder/biliary dz; Insulin receptors/Type 2 Diabetes; Pancreas/Type 1 Diabetes; Ovaries/infertility; Spit glands/Sjogrens; Myelin/MS; et cetera. How about Muscles/fibromyalgia? The Brain?? Consideration of complete wheat cessation is necessary I believe to prevent burning out multiple organs (including the coronary vasculature).

[The fatigue syndrome in autoimmune thyroiditis with polyglandular activation of autoimmunity][Article in Czech]
Zamrazil V et al.Vnitr Lek. 1998 Aug;44(8):456-60.

The authors compared in a group of 118 patients with autoimmune thyroiditis and a positive antibody titre against ovaries the grade of fatigue with the presence of organ specific and non-specific autoantibodies in the peripheral blood stream, antibodies against EBV and CMV, immunoglobulin concentrations, biochemical parameters of the lipid metabolism, glucose tolerance, ion balance and melatonin and serotonin levels. Patients with autoimmune thyroiditis were differentiated according to the degree of fatigue into three groups: 38 with fatigue typical for CFS (chronic fatigue syndrome), 30 with occasional fatigue and 50 without the feeling of fatigue. Fatigue of the CSF type was characterized by a significantly higher incidence of autoantibodies against the adrenals and a higher cholesterol level. Increased fatigue of the patients was associated with a lower melatonin level, a higher serotonin level and a lower M/S ratio as compared with patients without fatigue. In other indicators no differences were found. Fatigue in CFS could be associated, similarly as in autoimmune endocrinopathies, with impaired immunoendocrine regulation. In autoimmune thyroiditis, regardless of the concomitant presence of fatigue, in addition to antibodies against thyroid peroxidase most frequently antibodies against the ovaries were detected.
PMID: 10358448

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!

Coenzyme Q10 and the Ubiquinone System

I've been cleaning the house today and noticed BOY how much garbage and junk quickly accumulates. Often it's painful to face the facts... and the havoc and entropy!

You know... it's like the ol' coyboys in my favorite Western movies who needed a few shots of WHISKEY to take away the PAIN when the bullets were taken out of the wounds...

YIKES.

I have to admit I can't stand house cleaning. Allergic is a good word. I don't have asthma any longer (thanks to TYP and therapeutic doses of Vitamin D3) but I'm still allergic... CAN'T STAND IT. Some of my best friends and neighbors have let their 'professional' help go recently (with the increase in costs from PETROL etc)... I let mine go a year ago after we moved... Boy... can you spell M-I-S-E-R-Y...???

Occasionally I'll do this trick and invite my most Martha-Stewart-girlfriends over for dinner. I figure they can SHAME me into cleaning... of course it works and the house will be sparkling clean for about 10minutes...

Unfortunately sometimes I invite my friends over and I get busy and fail to have time to clean. I just hope that I can get them liquored up and blur their vision to the dirt rings in the toilet and the dust accumulating... NNNNAAAWWWWTTTT... they DON'T IMBIBE... what was I thinkin??!


How can a family of 6 generate so much waste? And one cat? And several house spiders?

For one, I've been losing some hair (though reversing after stopping my DARN synthetic hormone LNg for birth control) so... yeah go ahead make the dog comparisons... I admit I shed... Long hairs ALL OVER THE DARN HOUSE.

How does our mammalian bodies handle waste and garbage? Is it pollution? Or does everything to some extent get recycled???

Co Q10 helps with recycling of crucial antioxidants and vitamins in our mitochondria and membranes. Coenzyme Q10 is a crucial component of the TrackYourPlaque program.

Other benefits include:
--Counters the depletion of Co Q10 that occurs with Statin use
--Reduces Lipoprotein (a) 12% -- Check out the TYP Report
--Recycles our natural antioxidants like Vitamin E, Glutathione, etc
--Reverses heart failure--Plays an critical role in anti-aging, neuroprotection, cardioprotection and reduction in hyperinsulinemia/diabetes/MetSyn


Curr Neurovasc Res. 2005 Dec;2(5):447-59.The emerging role of coenzyme Q-10 in aging, neurodegeneration, cardiovascular disease, cancer and diabetes mellitus.Dhanasekaran M, Ren J.
Division of Pharmaceutical Sciences, School of Pharmacy, University of Wyoming, Laramie, WY 82701, USA.
Coenzyme Q (ubiquinone, 2-methyl-5,6-dimethoxy-1,4-benzoquinone), soluble natural fat quinine, is crucial to optimal biological function. The coenzyme Q molecule has amphipathic (biphasic) properties due to the hydrophilic benzoquinone ring and the lipophilic poly isoprenoid side-chain. The nomenclature of coenzyme Q-n is based on the amount of isoprenoid units attached to 6-position on the benzoquinone ring. It was demonstrated that coenzyme Q, in addition to its role in electron transport and proton transfer in mitochondrial and bacterial respiration, acts in its reduced form (ubiquinol) as an antioxidant. Coenzyme Q-10 functions as a lipid antioxidant regulating membrane fluidity, recycling radical forms of vitamin C and E, and protecting membrane phospholipids against peroxidation. The antioxidant property, high degree of hydrophobicity and universal occurrence in biological system, suggest an important role for ubiquinone and ubiquinol in cellular defense against oxidative damage. Coenzyme Q-10 is a ubiquitous and endogenous lipid-soluble antioxidant found in all organisms. Neurodegenerative disorders, cancer, cardiovascular diseases and diabetes mellitus and especially aging and Alzheimer's disease exhibit altered levels of ubiquinone or ubiquinol, indicating their likely crucial role in the pathogenesis and cellular mechanisms of these ailments. This review is geared to discuss the biological effect of coenzyme Q with an emphasis on its impact in initiation, progression, treatment and prevention of neurodegenerative, cardiovascular and carcinogenic diseases.

PMID: 16375724





Other illuminating references:

• Ernster L, Forsmark-Andrée P.
  Ubiquinol: an endogenous antioxidant in aerobic organisms.
  Clin Investig. 1993;71(8 Suppl):S60-5. Review.
  PMID: 8241707 [PubMed - indexed for MEDLINE]
• James AM, Smith RA, Murphy MP.
  Antioxidant and prooxidant properties of mitochondrial Coenzyme Q.
  Arch Biochem Biophys. 2004 Mar 1;423(1):47-56. Review.
  PMID: 14989264 [PubMed - indexed for MEDLINE]
• Mohora M, Katona E, Dinu V.
  Pro- and antioxidant functions of quinones in mammalian cells.
  Rom J Intern Med. 1999 Jan-Mar;37(1):3-14. Review.
  PMID: 15523940 [PubMed - indexed for MEDLINE]
• Albano CB, Muralikrishnan D, Ebadi M.
  Distribution of coenzyme Q homologues in brain.
  Neurochem Res. 2002 May;27(5):359-68.
  PMID: 12064350 [PubMed - indexed for MEDLINE]
• Shults CW.
  Coenzyme Q10 in neurodegenerative diseases.
  Curr Med Chem. 2003 Oct;10(19):1917-21. Review.
  PMID: 12871093 [PubMed - indexed for MEDLINE]
• Ernster L, Dallner G.
  Biochemical, physiological and medical aspects of ubiquinone function.
  Biochim Biophys Acta. 1995 May 24;1271(1):195-204. Review.
  PMID: 7599208 [PubMed - indexed for MEDLINE]
• Littarru GP, Tiano L.
  Bioenergetic and antioxidant properties of coenzyme Q10: recent developments.
  Mol Biotechnol. 2007 Sep;37(1):31-7. Review.
  PMID: 17914161 [PubMed - indexed for MEDLINE]
• Navas P, Villalba JM, de Cabo R.
  The importance of plasma membrane coenzyme Q in aging and stress responses.
  Mitochondrion. 2007 Jun;7 Suppl:S34-40. Epub 2007 Mar 16. Review.
  PMID: 17482527 [PubMed - indexed for MEDLINE]
• Siemieniuk E, Skrzydlewska E.
  [Coenzyme Q10: its biosynthesis and biological significance in animal organisms and in humans]
  Postepy Hig Med Dosw (Online). 2005;59:150-9. Review. Polish.
  PMID: 15928598 [PubMed - indexed for MEDLINE]
• Ernster L, Forsmark P, Nordenbrand K.
  The mode of action of lipid-soluble antioxidants in biological membranes. Relationship between the effects of ubiquinol and vitamin E as inhibitors of lipid peroxidation in submitochondrial particles.
  J Nutr Sci Vitaminol (Tokyo). 1992;Spec No:548-51. Review.
  PMID: 1297809 [PubMed - indexed for MEDLINE]
• Pobezhimova TP, Voinikov VK.
  Biochemical and physiological aspects of ubiquinone function.
  Membr Cell Biol. 2000;13(5):595-602. Review.
  PMID: 10987383 [PubMed - indexed for MED INE]
• Beyer RE.
  An analysis of the role of coenzyme Q in free radical generation and as an antioxidant.
  Biochem Cell Biol. 1992 Jun;70(6):390-403. Review.
  PMID: 1333230 [PubMed - indexed for MEDLINE]
• Nohl H, Gille L, Staniek K.
  The biochemical, pathophysiological, and medical aspects of ubiquinone function.
  Ann N Y Acad Sci. 1998 Nov 20;854:394-409. Review.
  PMID: 9928447 [PubMed - indexed for MEDLINE]
• Valko M, Leibfritz D, Moncol J, Cronin MT, Mazur M, Telser J.
  Free radicals and antioxidants in normal physiological functions and human disease.
  Int J Biochem Cell Biol. 2007;39(1):44-84. Epub 2006 Aug 4. Review.
  PMID: 16978905 [PubMed - indexed for MEDLINE]
• Nohl H, Gille L, Kozlov AV.
  Antioxidant-derived prooxidant formation from ubiquinol.
  Free Radic Biol Med. 1998 Oct;25(6):666-75.
  PMID: 9801066 [PubMed - indexed for MEDLINE]
• Merlo Pich M, Castagnoli A, Biondi A, Bernacchia A, Tazzari PL, D'Aurelio M, Parenti Castelli G, Formiggini G, Conte R, Bovina C, Lenaz G.
  Ubiquinol and a coenzyme Q reducing system protect platelet mitochondrial function of transfusional buffy coats from oxidative stress.
  Free Radic Res. 2002 Apr;36(4):429-36.
  PMID: 12069107 [PubMed - indexed for MEDLINE]
• Shults CW.
  Therapeutic role of coenzyme Q(10) in Parkinson's disease.
  Pharmacol Ther. 2005 Jul;107(1):120-30. Epub 2005 Apr 21. Review.
  PMID: 15963354 [PubMed - indexed for MEDLINE]
• Wold LE, Muralikrishnan D, Albano CB, Norby FL, Ebadi M, Ren J.
  Insulin-like growth factor I (IGF-1) supplementation prevents diabetes-induced alterations in coenzymes Q9 and Q10.
  Acta Diabetol. 2003 Jun;40(2):85-90.
  PMID: 12861406 [PubMed - indexed for MEDLINE]
• Rauchová H, Drahota Z, Lenaz G.
  Function of coenzyme Q in the cell: some biochemical and physiological properties.
  Physiol Res. 1995;44(4):209-16. Review.
  PMID: 8789639

The richest food sources of natural Coenzyme Q10:
--Organ meats: heart, liver, etc
--Fish, seafood, mollusks
--Meat: grass fed meat, poultry

Saturated Fats as Potent Anti-Atherogenic Drugs

I hope we are not still scarred by the long onslaught of ingrained sat-fat nonsense over the last few decades?

SCAR TISSUE from Red Hot Chili Peppers
ALBUM: Californication

Courtesy of Youtube.com

LAURIC ACID (12C MEDIUM-CHAIN SATURATED FATTY ACID) ASSOCIATED WITH RELATIVELY HIGHER HDL2b AND LOWER HDL3c

In the previous entry, conclusions from the same research below was discussed. They went further and looked at the lipoprotein subfractions including HDL2b and HDL3c. Mensink et al found that the higher the phospholipid transfer protein (PLTP) activity and the lower the cholesterol ester transfer protein (CETP) activity, the higher the relative abundance of HDL2b, the regression particle, and the lower the HDL3c, a small dense atherogenic particle. Lauric acid produced the highest ratio of PLTP to CETP activity when compared with the control, palmitic or oleic diets after 6-weeks.

Their assessment was "It is now clearly established that CETP and PLTP can modulate the size distribution of serum lipoprotein fractions. On the one hand, CETP can replace lipoprotein cholesteryl esters by hydrolyzable triglycerides which are derived from the triglyceride-rich lipoproteins, favoring the emergence of small-sized LDL, pre-beta-HDL and small-sized alpha-HDL [40]. On the otherhand, PLTP has been shown to promote the formation of both pre-beta-HDL and large-sized alpha-HDL through an inter-HDL fusional mechanism [40]. In the present study, no significant differences in the size distribution of either HDL or LDL fractions were observed in sera from subjects consuming either of the three experimental diets... Despite the absence of modifications of the size distribution of HDL, significant relationships between lipid transfer activities andthe relative abundance of HDL subpopulations were observed among (INDIVIDUAL) subjects consuming the same, standardized diet. Overall, CETP correlated positively with small HDL, but negatively with large HDL, whereas opposite tendencies were observed with PLTP that correlated negatively with small HDL, but positively with the large ones (ie, HDL2b)."

Variations in serum cholesteryl ester transfer and phospholipid transfer activities in healthy women and men consuming diets enriched in lauric, palmitic or oleic acids. Lagrost L, Mensink RP, Guyard-Dangremont V, Temme EH, Desrumaux C, Athias A, Hornstra G, Gambert P. Atherosclerosis. 1999 Feb;142(2):395-402. Email for PDF.







BALANCE OF CETP AND PLTP NECESSARY

Minimization and maximization, respectively, as the Mensink study showed.

What are the dangers of artificially inhibiting CETP and ignoring PLTP activity?

What are the dangers of raising only HDL3c (small dense atherogenic HDL) and lowering HDL2b (the regressive, large/fluffy HDL)??!

The story of Torcetrapib...is one with an extremely unhappy unending...

Well...for one Pfizer is now out of the lipid-heart-disease business (Lipitor® RIP 2011 when it goes generic). Read the TYP report on this CETP-inhibitor and the surprising outcome HERE. Pfizer's $20B Torcetrapib HDL-raising drug unfortunately failed big time (in low-fat, low cholesterol, low saturated fat populations). Not only was an increase of 50% in total HDL observed in humans but also coronary regression was demonstrated in animal studies. Oddly this curious drug was associated with nearly double the deaths in the single human morbidity/mortality trial. Are animal brains as functional or large as human brains? What is the purpose of cholesterol? Are humans brains not laden with cholesterol? In fact 23% of the whole body pool of cholesterol is found in the brain and central nervous system. Although the brain only weighs 2.1% of our total weight, the cholesterol content is the highest compared with any other tissue (23 mg chol/gram). How much cholesterol is in an egg yolk? A measly ~200 mg. Barely enough to support or maintain a smidgeon of your SUPER SAVANT BRAIN. And we're told to have no more than an egg a day? Can you spell autism? Well... probably neither can the great-grandchildren of the geniuses who proposed these low-cholesterol indictments. How many more generations will be affected by the policies propagating the low-fat hypothesis? Are we de-evolving as a species *hint....WALL*E *?

Thematic review series: Brain Lipids. Cholesterol metabolism in the central nervous system during early development and in the mature animal. Journal of Lipid Research, Vol. 45, 1375-1397, August 2004.





BIOACTIVE LIPIDS -- BEST BALANCE -- BETTER THAN Torcetrapib

Fish oil EPA + DHA and seafood naturally lower CETP activity (preventing cholesterol transfer) and power up PLTP (moving phospholipids out of lipoprotein fractions). I had a hard time locating any VAP/NMR data on effects of fish oil components EPA and DHA, but two studies below demonstrate the outcome of EPA and DHA ingestion in depleting phospholipids out of LDL and HDL particles.

(1) Small supplements of N-3 fatty acids change serum low density lipoprotein composition by decreasing phospholid and apolipoprotein B concentrations in young adult women. Terpstra AH et al. Eur J Nutr. 1999 Feb;38(1):20-7.

(2) The effect of dietary n-3 polyunsaturated fatty acids on HDL cholesterol in Chukot residents vs Muscovites. Astakhova T et al. Lipids. 1991 Apr;26(4):261-5.

Native Chukot Peninsula residents, in contrast to Muscovites, consume a diet rich in n-3 polyunsaturated fatty acids. This dietary peculiarity is reflected in differences in plasma lipid and apolipoprotein contents. The Chukot residents have lower contents of total cholesterol, triglyceride, LDL (low density lipoprotein) cholesterol and apolipoprotein B, but higher HDL (high density lipoprotein) cholesterol levels than do Muscovites. The apolipoprotein A-I levels were identical in both groups. A higher HDL cholesterol to apolipoprotein A-I ratio was determined in the coastline Chukot residents (0.52 +/- 0.01) than in Muscovites (0.43 +/- 0.01; p less than 0.01). In contrast to Muscovites, the coastline Chukot residents also had higher n-3 and lower n-6 polyunsaturated fatty acid percentages in plasma and erythrocyte lipids, and lower phosphatidylcholine and higher sphingomyelin or phosphatidylethanolamine levels in HDL2b and HDL3. The higher HDL cholesterol levels in the plasma of the coastline Chukot residents appears to reflect the higher cholesterol-scavenging capacity of their HDL. We conclude from this study that the regular consumption of dietary n-3 polyunsaturated fatty acids by the coastline Chukot residents decreased LDL cholesterol transfer from plasma to peripheral cells, and enhanced cholesterol efflux from cellular membranes toward HDL.

A WONDERFUL COMPREHENSIVE REVIEW THAT I *HEART*

Nagao K, Yanagita T. Bioactive lipids in metabolic syndrome. Prog Lipid Res. 2008 Mar;47(2):127-46.

"This review explores the physiological functions and molecular actions of bioactive lipids, such as n-3 polyunsaturated fatty acids, conjugated fatty acids, sterols, medium-chain fatty acids (LIKE SATURATED FAT LAURIC, CAPRIC, CAPROIC, CAPRYLIC ACIDS), diacylglycerols and phospholipids, in the development of metabolic syndrome. Dietary bioactive lipids suppress the accumulation of abdominal adipose tissue and lipids in the liver and serum, and alleviate hypertension and type 2 diabetes through the transcriptional regulation of lipid and glucose metabolism. "

[DRUM ROLL...] DIETARY SATURATED FATTY ACIDS ACT LIKE NIACIN

Fatty acids including saturated fatty acids also bind PUMA-G and HM74 receptors. This is the receptor family that Niacin binds to and exerts its potent abilities to regress plaque (raise HDL2b 200-300%, lower TGs 40-60%) and evoke its anti-inflammatory effects. See Table 1 full list of the range of ketone body and the saturated fatty acids and their relative receptor affinities.

Taggart A, Waters MG et al. (D)-beta-Hydroxybutyrate inhibits adipocyte lipolysis via the nicotinic acid receptor PUMA-G. J Biol Chem. 2005 Jul 22;280(29):26649-52. Full 'accelerated publication' PDF here.

Other fatty acids which bind this astounding receptor PUMA-G are in listing of decreasing potency:
--Hydroxy-butyrate (ketone bodies associated with exercise training and intermittent fasting)
--Lactate (by-product of anaerobic exercise, strength training, intense exercise like CALIfornication)
--Acetate (C2), Proprionate (C3)
--Decanoate (C10) = caprylic acid, a medium chain saturated fatty acid (MC SFA)
--Heptanoic acid (C7)
-- Butyrate (C4) = short chain saturated fatty acid from butter oil and produced by gut flora from ingested fiber like oat bran, pectin, etc
--Octanoate (C8) = capric acid, MC SFA
--Pentanoic acid (C5)
--Hexanoate (C6) = caproic acid, MC SFA
--Nicotinic acid (niacin, SLO-NIACIN, NIASPAN) -- binds with high affinity to HM74 receptors

Umbellularia CalifornicaTION

Received a call at the last minute from a co-worker offering a chance to run the Bothe-Napa State Park half-marathon that was sold out! My bib belonged to an Asian dude originally from South India (sshhhHHH! -- don't mention to the race owners). Scored a great workout (only 10K actually) and free cool wool socks...

The other trail running I've done was the Marin Headlands race a couple Aprils ago where the bluest-ever wildflowers were in a sea of blooms over magnificent green hills. Enviro-Sports does a fantastic job at picking breathtaking locales paired with perfect timing for optimum weather, temperature and picturesque views. Unlike the Marin Headlands, with the semi-drought we experienced here in Northern California, Bothe-Napa park had neither muddy streams nor any waist-deep creeks to cross *big grin* THANK GOD.

Here were the usual hazards associated with blazing through the forest at crazy breakneck speeds:
--branches -- poking EXACTLY out at eye level
--gravel, slippery dry leaves, uneven footing which promote face-plants, shin-plants and twisted ankles
--steep slopes similar to downhill skiing (great place to catch your breath unless your foot catches a raised root or rock which can send you straight to the ground)
--crossing shady creeks
--TICKS - my main challenge (Lyme disease is indigenous -- needed to avoid petroleum skin/hair products which apparently ticks are highly attracted to)

My 6'2" race partner didn't need to worry as much about face-plants because I reassured him his face was definitely higher up from the ground than my vertically challenged one.

With all the senses heightened and exhilarated (trying strongly to avoid planting my head), it was difficult not to be totally captivated and distracted by the intoxicating smell of the forest and a particular aroma I couldn't quite identify until another runner shared with me that the woodsy perfume was (!) BAY LEAF (umbellularia californica). I've often cooked with it (the commercial Mediterrean species laurus nobilis) but the leaves were usually impotent and I've frankly never noticed anything so wonderful as what I was stomping and crunching below my feet. The air off the fresh leaves on the trees below the dense canopy wafted off as we brushed past them. Were the valleys just one big room deodorant? Could one possibly thrash the body any better while immersing the senses in this astonishingly sensual aromatherapeutic experience? (Honestly, a nice side effect of being on the an evolutionary/paleo lifestyle and diet is despite going through the gauntlet (Crossfit, endurance events, whatever), I rarely ever experience muscle aches or soreness afterwards. It defies bio-physics.)

My daughters love Pokemon and here is a creature they haven't discovered yet named after this fascinating spice:
BAYLEEF

Bayleef (ベイリーフ, Beirīfu?, Bayleaf in original Japanese language versions) is the evolution of Chikorita and first appeared in Pokémon Gold and Silver. It has a pale yellow body supported by four legs and a rather long neck and tail. On top of its head is a single large leaf. Its most defining trait is the "necklace" of seven tubular leaves that is located around its neck. Each of these curled up leaves contains inside it a tree shoot. From these leaves wafts a spicy scent that has stimulating properties. It can cheer people up, restore their health, make them more energetic and even heighten their drive for competition.

Have you ever purchased bay leaves from the grocery spice aisle? One ounce costs more than M A R I J U A N A... j/k. Don't forget I'm a legal drug-dealer (ie, board-certified-doctor-of-pharmacy) . . . not the other. Seriously, the stuff we buy where the volatile oils (known as eugenol) are mostly degraded by storage and age doesn't hold anything against the REAL STUFF. After the race I wanted to go back and stuff leaves into my wet sweaty bra but I r e s i s t e d the urge I'm proud to tell y'll. State property after all!

Why did humans ever evolve cooking and spicing up our food with this wonderful herb? Why do the French tie bouquet garnis in their fragrant kitchens?? How did Greeks and ancient Romans find power in rewarding victors with wreaths of laurel/bay leaves? What do Indians and Persians favor in their biryani (rice)? Mexicans in their delish nutrish menudo?

Remarkable antimicrobial properties exist in all spices and herbs and bay leaves are no exception.

• Friedman M, Henika PR, Mandrell RE. (From the local USDA Albany laboratories)
  Bactericidal activities of plant essential oils and some of their isolated constituents against Campylobacter jejuni, Escherichia coli, Listeria monocytogenes, and Salmonella enterica.
  J Food Prot. 2002 Oct;65(10):1545-60.


• Lee SY, Jin HH. Inhibitory activity of natural antimicrobial compounds alone or in combination with nisin against Enterobacter sakazakii.
  Lett Appl Microbiol. 2008 Sep 15.


• Rojo L, Barcenilla JM, Vázquez B, González R, San Román J.
  Intrinsically antibacterial materials based on polymeric derivatives of eugenol for biomedical applications.
  Biomacromolecules. 2008 Sep;9(9):2530-5.


• Raybaudi-Massilia RM, Rojas-Graü MA, Mosqueda-Melgar J, Martín-Belloso O.
  Comparative study on essential oils incorporated into an alginate-based edible coating to assure the safety and quality of fresh-cut Fuji apples.
  J Food Prot. 2008 Jun;71(6):1150-61.


• Di Pasqua R, Betts G, Hoskins N, Edwards M, Ercolini D, Mauriello G.
  Membrane toxicity of antimicrobial compounds from essential oils.
  J Agric Food Chem. 2007 Jun 13;55(12):4863-70.


• Viyoch J, Pisutthanan N, Faikreua A, Nupangta K, Wangtorpol K, Ngokkuen J.
  Evaluation of in vitro antimicrobial activity of Thai basil oils (INCL EUGENOL) and their micro-emulsion formulas against Propionibacterium acnes.
  Int J Cosmet Sci. 2006 Apr;28(2):125-33.


• Gaysinsky S, Taylor TM, Davidson PM, Bruce BD, Weiss J.
  Antimicrobial efficacy of eugenol microemulsions in milk against Listeria monocytogenes and Escherichia coli O157:H7.
  J Food Prot. 2007 Nov;70(11):2631-7.

Eugenol apparently lowers stress-related cholesterol in experimental animals as well as attenuating/reversing red-blood-cell membrane dynamics (Valdman AV et al, Indian J Exp Biol. 1992 Jul;30(7):592-6).

The first and only IPO I bought in high school was Calgene I'm sad to confess (f o o l I was...AND still am after missing GOOGLE). Talk about GMO-frankenfood monstrosities. *sigh* Perhaps, however, they've mildly redeemed themselves... somewhat. Their research on the California bay leaf enzyme called 12:0-ACP thioesterase shed light on it's involvement in lengthening the carbon chain in saturated fatty acids in the flowers (ie, seeds -- the reproductive parts) and leaves (less activity). Apparently the seeds of the California bay leaf tree are rich in lauric acid, the medium 12-carbon chain saturated fatty acid.

Voelker TA et al. Lysophosphatidic acid acyltransferase from coconut endosperm mediates the insertion of laurate at the sn-2 position of triacylglycerols in lauric rapeseed oil and can increase total laurate levels. Plant Physiol. 1999 Jul;120(3):739-46.Hawkins DJ et al. Modification of the substrate specificity of an acyl-acyl carrier protein thioesterase by protein engineering.Proc Natl Acad Sci U S A. 1995 Nov 7;92(23):10639-43.

Graham IA et al. No induction of beta-oxidation in leaves of Arabidopsis that over-produce lauric acid. Planta. 1999 Jan;207(3):385-92. (Plants generate energy via beta-oxidation of fatty acids just as animals do!)


Why do we love lauric acid ? For heart disease, immune protection and optimization and overall health?

Lauric acid lowers Lp(a)... particularly in men (44%; non-statistically significant). See below Table.

• Temme EH, Mensink RP, Hornstra G. Comparison of the effects of diets enriched in lauric, palmitic, or oleic acids on serum lipids and lipoproteins in healthy women and men. Full PDF here. Am J Clin Nutr. 1996 Jun;63(6):897-903. PMID: 8644684

Lauric acid also raises HDL -- the plaque-regression-related subfraction (and cancer protective particle). Please see Table 5 -- at the top. In a short six-weeks, lauric acid increased total HDL by:

-- 16.7% for men (baseline: HDL = 1.26 mmol/L = 48.7 mg/dl) which appears to correlate well with Lp(a) reduction! Though hard to tell with Lp(a) varying in the deviations and this study population too small for any significance or actual comparisons.

-- 5.6% for women (baseline: HDL = 1.58 mmol/L = 61.1 mg/dl; TG=82.3 mg/dl)



In the below research conducted by the same group, they found that "Nevertheless, lipid transfer activities correlated significantly with the relative abundance of HDL2b, HDL2a, HDL3b, and HDL3c with phospholipid transfer activities. In general, serum phospholipid transfer protein (PLTP) activity correlated positivly with HDL cholesterol after the dietary interventions...serum PLTP activity, as measured as the rate of radiolabeled phosphatidylcholine transferred from liposomes toward serum HDL, was significantly higher with the lauric acid diet (23.5+/2.6%) than with the palmitic acid diet (22.5+/-2.5%) (P = 0.0013)."

• Lagrost L, Mensink RP, Guyard-Dangremont V, Temme EH, Desrumaux C, Athias A, Hornstra G, Gambert P.
  Variations in serum cholesteryl ester transfer and phospholipid transfer activities in healthy women and men consuming diets enriched in lauric, palmitic or oleic acids.
  Atherosclerosis. 1999 Feb;142(2):395-402.

Food sources rich in lauric acid are:

• unrefined coconut oil (40-50%)


• unrefined palm oil


• butter oil (greenpasture.com) -- contains also butyrate (ligand for the niacin-receptor), CLA, Vitamin K2, LDL-lowering Plant Sterols, Vitamin A/D/E, omega-3 ALA, etc. Read Weston A. Price.


• human breastmilk (not my highest recommendation *wink*)


• (umbellularia californica seeds and flowers... probably other herbal seeds too but haven't had time to verify)

Warrior Training -- Sustain a STRRIDE

These Duke University cardiologists performed an RCT (randomized controlled trial) on exercise intensity and frequency and found that large big puffy HDLs are can be achieved with exercise and can be degraded by 'de-training'. They found "In conclusion, physical inactivity has profound negative effects on lipoprotein metabolism. Modest exercise prevented this. Moderate-intensity but not vigorous-intensity exercise resulted in sustained VLDL-triglyceride lowering. Thirty minutes per day of vigorous exercise, like jogging, has sustained beneficial effects on HDL metabolism."


Inactivity, exercise training and detraining, and plasma lipoproteins.

STRRIDE: a randomized, controlled study of exercise intensity and amount.
Slentz CA, Houmard JA, Johnson JL, Bateman LA, Tanner CJ, McCartney JS, Duscha BD, Kraus WE. J Appl Physiol. 2007 Aug;103(2):432-42.
Division of Cardiology, Duke Univ. Medical Center, Durham, NC 27710, USA.

Exercise has beneficial effects on lipoproteins. Little is known about how long the effects persist with detraining or whether the duration of benefit is effected by training intensity or amount.


METHOD OF MADNESS: Sedentary, overweight subjects (n = 240) were randomized to 6-mo control or one of three exercise groups:

1. High-amount/vigorous-intensity exercise (equivalent to jogging 20 miles/wk (32.0 km) at 65-80% max effort -- approx 10,000 steps 4 days per week)
   
2. Low-amount/vigorous-intensity exercise (equivalent to jogging 12 miles/wk at 65-80% of max effort)
   
3. Low-amount/moderate-intensity exercise (equivalent to walking 12 miles/wk (19.2 km) at 40-55% of max effort) -- THIS IS THE TRACK YOUR PLAQUE MINIMUM. Remember...all things in moderation except love and laughs.

Training consisted of a gradual increase in amount of exercise followed by 6 mo of exercise at the prescribed level. Exercise included treadmill, elliptical trainer, and stationary bicycle. The number of minutes necessary to expend the prescribed kilocalories per week (14 kcal x kg body wt(-1) x wk(-1) for both low-amount groups; 23 kcal x kg body wt(-1) x wk(-1) for high-amount group) was calculated for each subject. Average adherence was 83-92% for the three groups; minutes per week were 207, 125, and 203 and sessions per week were 3.6, 2.9, and 3.5 for high-amount/vigorous-intensity, low-amount/vigorous intensity, and low-amount/moderate-intensity groups, respectively. Plasma was obtained at baseline, 24 h, 5 days, and 15 days after exercise cessation.


ROARING RESULTS: Continued INACTIVITY resulted in significant increases (bad) in the control group:
(Do you think plaque progressed? HEYYLLL Y E A H)
--low-density lipoprotein (LDL) particle number
--small dense LDL--LDL-cholesterol
--weight gain (1kg = 2.2 lbs)
--body fat increases (8.6% abdominal belly fat increase in 6mos)


A modest amount of exercise training prevented this deterioration (good).

Moderate-intensity but not vigorous-intensity exercise resulted in a sustained reduction in very-low-density lipoprotein (VLDL)-triglycerides over 15 days of detraining (P less than 0.05)

WOW. Yup not bad, eh? Moderate intensity was actually just as good the vigorous activity for reducing weight, in fact, was better for these untrained/sedentary individuals for de-training VLDL-TGs and body fat reducations. This is my experience as well -- I need long sustained, moderate intensity exercise to burn (stubborn) fat and maintain weight. Obviously the longer duration the better, and either intensities in the trial were better than nothing. Here the graph exemplifying the benefits of moderate intensity for belly fat reduction over vigorous intensity (see bottom bar graph). Low amounts of moderate produced a reduction of 1.2% subcutaneous belly fat compared with a 3.1% increase in the low amount vigorous group.

Here the authors report the precise changes in body fat in the STRRIDE study Kraus WE et al J Appl Physiol 2005 Oct;99(4):1613-8: HERE

Their conclusions from this analysis: "The equivalent of 11 miles of exercise per week, at either intensity, prevented significant accumulation of visceral fat. Controls gained visceral fat (8.6% BF +/- 17.2%; P = 0.001) in 6 months. Significant gains in visceral fat over only 6 mo emphasize the HIGH COST OF CONTINUED INACTIVITY. A modest exercise program, consistent with recommendations from the Centers for Disease Control/American College of Sports Medicine (CDC/ACSM), prevented significant increases in visceral fat." The highest exercise group lost ~ 7% body fat in only 8 months. Roughly approx one inch off the inches measured at our belly button (umbilical) is equivalent to approx 1% body fat. My personal experience mirrors these experimental measures. At moderate intensity which is equivalent to ~ 60% of our peak oxygen output, we our maximally in our aerobic fat-burning mode. Our muscles' (including the heart muscles) preferred energy source is fatty acids -- these are the longest burning 'logs' that fuel moving muscles. Sustained moderate intensity movement draws from our fat reserves the most optimally. Now, with that said, we do require a little intensity in life. My trainer once told me at the end of the workout, push the intensity to 70-80% for 1-2 minutes for speed and power later. Adding strength training and weights potentiates strength and burns visceral fat further (toxic fat enclosing our viscera/offal/organs, livers/gallbladders/hearts/etc). So minimum 11 miles per week? And for maximum gluteus maximus, squats + walking 20 miles per week?

The high-amount group had significant improvements in ALL the benefits below that were sustained for 15 days after exercise stopped:
--high-density lipoprotein (HDL)-cholesterol
--HDL particle size
--large HDL levels

The more, the better the HDLs.

Modest WALKING 10,000 steps most days... INTENSE PLAQUE BUSTING POWER!
I like that. And the benefits can be sustained and uncompromised despite times when I can't get off my beautiful bum.

I really really really like T H A T .

Group Three is what we try to attain at the Track Your Plaque program at the mininum. But after conditioning and some practice, a moderate amount at moderate intensity is preferred for its lipoprotein-shifting, insulin-sensitizing, mood-elevating, stress-busting benefits.

Use a pedometer. Gradually work up to an ultimate goal of walking (not jogging) 10,000 steps per day. More details HERE at TYP.

Walk. Sustain a STRRIDE.

Sixty minutes at 60% of max effort for 6 days of the week. 60-60-6. Sound familiar? 60-60-60-60 Rules for Regression.

Is that devil-talk?

We are not talking 'elite' athlete training or even amateur-weekend-athlete training. We are talking from an untrained, sedentary, have-not-exercised-since-Reagan-was-in-office perspective.

Aim to start LOW and go SLOW.

Take time to build up tendons, ligaments, strengthen joints and condition the lungs and other apparatus. Always warm up for the minumum 10-20 min in order to prevent injury or pulling a hamstring (my Achilles -- this used to frequently happen to me and derail training for 3-4mos -- but not now with squat exercises *smile* luv em). With the weather cooling now, warming up consistently and regularly will be the key to sustaining a program without disturbing injuries which would undoubtedly halt any well-intended program.

If you have not embarked on an exercise program before, then start first by asking your physician/cardiologist for an exercise stress Thallium to first assess flow, ischemia and changes on EKG. It is prudent for even well-trained elite athletes to undergo this test as well (as many have done and reported at the TYP forum) to make sure no underlying asymptomatic pathologies exist.

FINAL CONCLUSIONS: In conclusion, physical inactivity has profound negative effects on lipoprotein metabolism. Modest exercise prevented this. Moderate-intensity but not vigorous-intensity exercise resulted in sustained VLDL-triglyceride lowering. Thirty minutes per day of vigorous exercise, like jogging, has sustained beneficial effects on HDL metabolism. PMID: 17395756