(NSFW) B**bies, B**bies, B**bies... I see..chopped off b**bies

Sunny Tales

Sunlounger

If you know me (and this blog) you know I love racks and b**bies (incl mine).

So it is exxxtremely disheartening when I hear of individuals choosing to go through the agony of cortisol-spiking surgeries to remove their respective rack and b**bies. Now that Jolie' preventive bilateral mastectomay has hit the big news, I see chopped off b**bies and ovaries everywhere. [Cue: Sixth Sense movie music]

Sayonara b**bies

LOL. The horse and I will miss the real thang

Breasts and B**bies: Chock Full of Both Omega-3, MCT (medium chain triglycerides) and Taurine

Our breasts serve an evolutionary function as storage for all the goods things that need to be passed to the next generation, besides adipose storage and breastfeeding. Omega-3 fatty acids from seafood, grassfed game, herds, and free range poultry are selectively stored in breast, gluteal, abdominal and thigh fat. And the amount that gets stored in the breasts and other fatty tissues is governed in a dose-dependent fashion over time. The nutrients in the breast are important not only for lactation (year 1-2 for newborns) but also for gestation.  Our breasts become factories to feed the next generation all the things that nourish and grow the massive homo sapien brain and forward-gazing, stereoscopic, color vision, X-ray eyeballs, which doubles in physical size during the first 12 months of life. The contents of breast milk are super foods for newborns: MCTs (caprylic acid, lauric acid), omega-3 fatty acids (EPA + DHA), taurine, vitamin A, vitamin D, magnesium, zinc, iodine, colostrum, amino acids, galactose, IgM, immunoglobulins, protective enzymes, epidermal growth factor, etc. For certain nutrients, naturally, maternal supplementation also works when the mom cannot breastfeed (hormone imbalances, anatomical issues, neonatal twisted tongue, etc).

A baby is born with inherent 'leaky gut' (intestinal permeability) for the first few months in order for some of the larger protein molecules and mom's immunity to pass directly into their blood stream for immunoprotection. Since the baby has an underdeveloped and immature immune system, there is no point in vaccinations (full of toxic aluminum or mercury) on Day 1 of life (assinine).

Many factors in breastmilk subsequently raise of the IQ of newborns who breastfeed.  In one study, the breastmilk (not necessary connected with the close maternal-baby contact, milk in tube) was associated with a 8.3 point increase in IQ testing in preterm children at age 7.5-8 years of age compared with no breastmilk.

See prior animal pharm:  MCT Oil (coconut oil, breastmilk) kick the crapola out of olive oil

Credit: Celeb*tchy

higher? harder? pointier?

Good job Kristi Funk MD

On Nursing

"Its unique recipe of fatty acids boosts brain growth and results in babies with higher I.Q.'s than their formula-slurping counterparts. Nursing babies suffer from fewer infections, hospitalizations and cases of sudden infant death syndrome. For the mother, too, breast-feeding and its delicate plumbing of hormones afford protection against breast and ovarian cancers and stress. Despite exhaustion, the in-laws and dirty laundry, every time we nurse our babies, the love hormone oxytocin courses out of our pituitaries like a warm bath. Human milk is like ice cream, Valium and Ecstasy all wrapped up in two pretty packages."  Source:  NYT Toxic Breast Milk?

Credit: NYT Toxic Breast Milk?

Breastfeeding: Good way to detox pesticides, metals and PCBs (flame retardants)

Unfortunately our breasts store both the good and the bad... our fatty breast tissues are magnets and reservoirs for fat-soluble toxins and heavy metals from our produce (pesticides), commercial meat (growth hormones, pesticides), marine fish and seafood, pharmaceuticals (aluminum antacids, mercury/Al from vaccines, etc), dental (mercury and other metals from amalgam and titanium dental implants), Teflon cookware and coated clothing (PFOA), and environment (flame retardants, mercury/arsenic from coal burning plants which supply 40-50% of USA energy, aluminum from municipal water, blah blah blah).  The individuals who are least likely to have the biochemical mechanisms to chaperone and eliminate these modern industrial toxins, are the individuals most highly likely to develop inflammatory conditions including cancer, autoimmune diseases and Western chronic diseases.

Some of the identified genetic variants are MTHFR (Amy Myers MD), GSTM1 (Mark Hyman MD), COMT, ApoE4, CBS, GSTT, BRCA1/2, and several other emerging ones. A functional medicine doctor and dietician, Dr. Elizabeth Boham MD talks about how she developed breast cancer in her 30's despite 'doing all the right things' eating low fat, exercising regularly, etc HERE. She talks about how to identify and remove toxins in our food, lifestyles and environment.  A functional medicine and SNP case study: 'George'. To see more on SNPs and diverse associated human diseases, go into OMIN (online Mendelian inheritance in man), RegulomeDB.org/GWAS and PrometheASE.

Who has pesticides and PCBs in their toxome?  Apparently everyone -- adults and newborns before even their first breath of air according to CDC, NHANES and EWG studies. Even the President's Panel reported so in 2008.

In the '80s and '90s apparently Europe cracked down and starting banning dousing all home furnishings and clothing products with flame retardants (PCB and its cogener, polybrominated diphenyl ethers, PCBEs). Not the case in the USA.  In California for several decades, PCBs were required on pajamas, pillows, mattresses, couches, etc and thus many other states (and China) have followed suit.  PCBs end up in the ocean and rivers and marine life especially large predators bioaccumulate PCBs, mercury, dioxins, and pesticides. Cats and other indoor pets (and children) inadvertently consume dust and lick their fur, subsequently becoming exposed to PCBs.  All of our cats unfortunately developed endocrine disorders and I can never be certain that it was not secondary to the PCBs in their seafood/tunafish soft food that we 'treated' them with (combined with BPA-lining of the catfood cans).  They were all healthy and fine until 3-9 months after introducing them to seafood canned catfood....

In 'A retrospective study of PBDEs and PCBs in human milk from the Faroe Islands' the authors tested and tracked flame retardants in the milk from women who live on the Faroe Islands. They concluded 'Although remote from pollution sources, the Faroe Islands show high concentrations of POPs in human milk, particularly PCBs, but also PBDEs. The PBDEs show increasing concentrations over time.'

From Dr. Pizzorno in Is Toxin Exposure Relevant?

We know that considering the effect of one chemical at a time is no longer suficient. The Centers for Disease Control (CDC) published data on the levels of selected persistent organic pollutants (POPs) – a category of toxins which includes dioxins, phthalates, PDBEs, PCBs, etc. – and found that among a representative sample of the US population, some toxins were present in essentially every individual over the age of 12, including, for example, p,p’-DDE and hexachlorobenzene.5 An analysis of NHANES data found up to a 38-fold adjusted increase in risk for diabetes prevalence in those with the highest levels of 6 POPs,6 and increased risk has also been documented for cardiovascular disease,7 insulin resistance, impaired neurological development, learning and attention deicit disorders, endometriosis, and deficits in the hypothalamic-pituitary-thyroid axis8,9,10,11 (Figure 1 shows the increasing concentration of PBDEs (polybrominated diphenyl ethers) in breast milk).12 While very little data for humans is available, current evidence suggests that PDBEs are likely to be developmental neurotoxins, and are likely to have synergistic effects with similar chemicals.13

In addition to exogenous toxins such as POPs and heavy metals, a number of endogenous substances also require efficient functioning of detoxification enzymes to prevent a build-up of harmful metabolites. For example, endotoxins from bowel flora have been associated with depression, chronic fatigue, inflammatory bowel disease, and atherosclerosis, effects partly influenced both by bacterial species as well as intestinal permeability.14,15,16,17,18 Also, catechol estrogens and estrogen quinones are estrogen derivatives associated with oxidative damage and reproductive tissue cancers, which accumulate due to alterations in enzymatic activity.19,20 Other examples are the build-up of methylmalonic acid and homocysteine - both metabolic by-products known to have vascular, renal, and neurological toxicity, consequences of genetic susceptibility and poor B vitamin status.21,22,23,24

What Can We Do?

We must do much.  The statistics for lifetime sporadic cancer risk is currently 1:3 and will exponentially increase to 1:2 by 2020 according to WHO statistics.  I believe it.  Our toxome is excessive and unfortunately no diet (even paleo or ancestral diets) frees us from the pollution and the body burden accumulated over generations (our mothers, their grandmothers and, particularly, this current one).  We can thank the World Wars which ushered in technology (nitrogen fertilizers, Agent Orange).  It is rather wicked and ironic that the best green for liver support and thus elimination of pesticides, metals and PCBs is dandelion greens (e.g. a weed) introduced to the Americas by the British.

Good luck as we shall all need it.

Credit: Regul Toxicol Pharmacol. 2006 Apr;44(3):249-61.

See other animal pharm:
BRCA 1/2 Myths and Measuring Oxidative DNA Damage, 8-OHdG
USA Cancer Management: 50 Shades of F%$*# UP

Other resources:
Our Feel-Good War on Breast Cancer
Dr. Cate, BRCA Testing: Are the Medical Options Sensible
Mercury: How to Get This Lethal Poison Out of Your Body
How to Rid Your Body of Mercury and Other Heavy Metals: A Three-Step Plan To Recover Your Health
Kaayla Daniel and Galen Knight (WAPF) -- Oral Chelation and Mercury/metal-free Living (How to Avoid Toxic Metals and Clear Them From The Body)
Soy Recovery: The Toxic Metal Component
The Little Known Soy Gluten Connection
WAPF -- Environmental Toxins (comprehensive list of Wise Tradition articles)
Toxic Ignorance and Right-To-Know Biomonitoring

Ancestral Allele ApoE4: Super Brain Power, Fertility, Lipophilic Immunity

Ancestral Nutrition: The Imperfect Diet Cleaves Adaptive Genetic Polymorphisms

Hat tip to B. Pottenger for the latest science daily (HERE) on the importance of ancestral, customized nutrition for our health. Chilton et al found desaturase/FADS variants in African Americans which take medium chain n-6 PUFAs (polyunsaturated fatty acids) and convert them into long chain n-6 PUFAs, like arachidonic acid which may increase systemic inflammation. They purport this may explain the inordinate increase in Western diseases observed in African Americans who display a certain FADS genotype variant for fatty acid disposal when they eat the high n-6 PUFA Western diet, including prostate cancer, diabetes, diabetic complication, heart attacks, obesity and dementia/Alzheimers. [I edited the last post -- continental Africans also have a high rate of apoE4 in addition to current hunter-gatherer groups in Africa.]








ApoE4, The Ancestral Allele = Carnivorous and Fatty Acid-Adaptive Allele

It is clear that our ancient hominid predecessors had something special that allowed them to leave Africa ~2 mya and navigate the terrain and uncertain food, energy and climate allotments. Like others I subscribe to the marine hypothesis (Cunnane SC) that certain brain nutrients are essential for IQ and brain function. Both Cunnane and Jonathon CK Wells writes about the 'fattiness' of the human brain and how this factored into our brain evolution and global domination of every potential ecological niche... not withstanding the moon and interplanetary travel as well. Wells' book 'The Evolutionary Biology of Human Body Fatness: Thrift and Control' details the fats that built our history and brains.

A couple evolutionary biologists also assert that the APOE4 allele is our 'meat-adaptive' gene. Well. This makes sense to a finite degree however no research that I could find illustrates apoE increasing proteins into the brain or digestion... On the other hand, the research is highly demonstrative of apoE4 increasing FATTY ACIDS into our brains, mitochondrial metabolism and enhancement of neural efficiency.

My view:
apoE4 -- Infiniti of cars (same Nissan engine), running on super premium fuel (ancestral allele)
apoE3 -- Nissan Maxima (wild type allele), runs both regular and premium fuels
apoE2 -- Nissan Sentra, on regular unleaded (agarian allele??)
apoE combos -- Prius hybrids (phenotype varying by degrees)

One change of the protein structure of apoE at the 61 spot from T to R/arginine may have set the stage for evolution of other nervous system and housekeeping genes that not only grew a superior engine in the brain but also the chassis/architecture of our hard drives. The ancestral apoE4 allels may be one among several genetic variations that sets us vastly apart from our not so distant primate past.







Super Brain Power + Super Brain Fuel

Though in the medical literature is rife with negative associations between apoE4 and a variety of conditions, my observations are that in those who exhibit high LDLs appear to display the most supreme levels of super-healing and extraordinary intelligence. See Hyperlipid (Peter D. for studies where high LDL associated with positive improvements and longevity, HERE J-LITT. Please also review the neurobio series on Alzheimer's by the wonderful Emily D. at Ev Psych and how low cholesterol is associated with lower cognition HERE.

As you can see from Mahley and Rall's 2000 publication, LDL sharply corresponds to apoE status. E4, the highest; E2, the lowest LDL. Do most cardiologists know this as they prescribe cookie-cutter NCEP/ATPIII-aligned statins? Please.

The density of the LDL determines its function. Small dense is damaging. For E4, dietary carbohydrates and dietary deficiencies of saturated fat dramatically shape and create small, dense, harmful LDL particles. The only rare cases of coronary calcification improvement on EBCT at a coronary heart website were the uncommon participant on a lower carb, HIGH SATURATED FAT intake. E4 appear exquisitely more sensitive to diet, exercise, fats/carbs and environmental toxicants.

Mondadori et al used new technology fMRIs to brain scan young chess-playing individuals and compared their the apoE status. The apoE4 showed increased memory, retrieval, neuropsychology and apparently neural efficiency. E4 indeed appear to run their brains on better fuel, e.g. fatty acids, the currency of nervous system cells.

Why is this not observed in E4 carriers in older age in the industrial populations? In the prior post, researchers discussed how the cysteine amino acid is lacking in E4, at the 112 site. E2 has 2 cysteine's per allele; E3, 1 cysteine; E4, N-O-N-E. This protein conformation apparently stupendously reduces the capacity for apoE to shuttle trace metals out of nervous system tissues. Many enzymes regulate and control metals in the brain however having the E4 allele is like a neuronal death sentence in a world that is contaminated by metals, not excluding one's own oral cavity. Sources of neolethal metal: dental amalgams (50% are mercury which gas off), stents, ortho/dental implants, well water, water purification at municipal plants (alum/Al), lead from leaded fuel/diesel, copper piping, fish intake (the EPA advises pregnant women limit fish, shouldn't we non-pregnant as well?), vaccines (Hep B, flu, whooping cough, Td, etc) and broken Hg thermometers.




Super Fertility = (Pre-Industrial) ApoE4 Populate the World

The literature abounds with cases of higher infertility in apoE4 women. FYI All literature needs to be viewed from an evolutionary perspective and in this context the great majority of these studies for me only demonstrate that the Western diet/lifestyle are particularly adverse to the hunter-gatherer types who carry the E4 allele. If a person carries the E4, then consuming an anti-HG diet (e.g. refined, non-ancestral), then the preponderance of small dense, oxidizable LDL and a hyperactive immune system which searches and scars, yes of course, will result in higher rates of infertility, fibroids, ovarian cysts, PCOS and less pregnancies, as countless PubMed articles report.

One study looked at HG super fertility... In African-Ecuadorians and a HG group, Capaya Indians, indeed the # of gestations and pregnancies were astoundingly higher in E4 carrier women. See citation below Corbo et al. They hypothesize that higher rates of sex hormone steroidogenesis can potentially occur with the E4 genotype.

My own family may also be a prime example. On low carb, mod-high sat fat, my LDLs are greater than 130s which is 'high' for the medical establishment, EVEN THOUGH THE HDL-CHOLESTEROL ECLIPSES THE S.A.D. HDL for women at 105 mg/dl. Both my father and stepmother's side each have 12 children (with 1-2 nonsurviving siblings). How is this humanly possible, as a mom, I used to WONDER OUT LOUD IN HORROR. I think Catholic families might relate... I could have a litter kids if I didn't have a brakestop. My parents and step mother are from an ancient nomadic group (Hakka, part of Han) and in all likelihood harbor the E4 allele somewhere, as my LDLs my appear to indicate. Each of my siblings and I (4 total) have had an autoimmune disorder and are somewhat sensitive to modern pollution and toxicants (gluten, dairy/casein, medications, and sulfa-, nickel-, metal-allergies).




Super Immunity

In a seminal article in PNAS, Caleb Finch's 'Evolution of the human lifespan and diseases of aging: Roles of infection, inflammation, and nutrition' talks about how humans evade infections and the role of apoE4. As a carnivorous creature, hominids had access to ingestion of better protein, trace minerals and fats. The apoE system shuttles cholesterol and the contents of LDL and HDL particles into nervous system tissues (iodine, zinc, tocopherols, ubiquinone, vit K2, etc).

By absorbing fats from the intestines quickly, this sequesters fat from parasites, bacteria and other pathogens. It is believed this might be one mechanism of super immunity which is observed in E4 carriers. Finch and Stanford (QJB, 2004) report 'In chronic infections by hepatitis C virus (HCV), apoE4 carriers had milder liver disease (Wozniak et al. 2002). The protection against HCV by apoE4 is consistent with the role of lipoproteins in transmission of HCV and other viruses (Wozniak et al. 2002), and fulfills hypotheses that apoE4 is a resistance factor for lipophilic parasites (Martin 1999) and that apoE4 confers advantages in early life (Charlesworth 1996). ApoE may also influence infections by other viruses and by prions, but the evidence is less clear (Table 3, Note 1d and Appendix).'




Human Migration: Evolution of Machinery to Convert Saturated Fat into Omega-3 PUFAs

How did humans go so far north, such high altitudes where seemingly harsh climate and terrains existed? Many SNP variants have apparently evolved which helped our ancestors thrive and live very full lives in certain microecological niches on earth. One thing that has baffled me to know end is the apparent n-3 pufa sources in northern Europe, Africa or northern China as hominids moved there 200,000 years ago. The FADS gene clusters of polymorphisms definitely explains a lot as to how the delta 5 and 6 desaturases control elongation of fatty acids to the ever important essential brain nutrient n-3 pufa.

Terrestrial Brain nutrient allocation and Adaptation from Sahara marine-sources (hypothesis):
EPA DHA n-3 pufa: ???! from where, ?megafauna and small animal predation
ALA n-3 pufa: wild greens
Iodine: ApoE4, possible iodine-oral cavity cellular conservative adaptations, polymorphs of MT1,2,3
Zinc: ApoE4
Magnesium: ApoE4
Taurine: Raw megafauna hunt successes, small animals, fish/seafood from local rivers/tributaries
UVB induced vitamin D: grubs, lighter eyes, lighter skin, melanin reduction, megafauna livers
Red wine: j/k


In a prospective human intervention trial, Dabadie et al gave myristic acid, a 14 carbon SATURATED FATTY ACID, to humans and showed an increase and significant enrichment of DHA, omega-3 pufa, in tissues. The authors later performed another study, increasing the myristic and giving ALA and found a J- or U-shaped curve where less DHA changes were seen at higher saturated fat intakes.

I think this is the first and only study that I could find where saturated fat can be under the influences of our desaturases to produce and synthesize a necessary and essential brain long-chain omega-3. Lard is 1% myristic, the head oil of sperm whale 15% and dairy fat 10%.






Citations

1. The impact of FADS genetic variants on ω6 polyunsaturated fatty acid metabolism in African Americans. Mathias RA, Sergeant S, Ruczinski I, Torgerson DG, Hugenschmidt CE, Kubala M, Vaidya D, Suktitipat B, Ziegler JT, Ivester P, Case D, Yanek LR, Freedman BI, Rudock ME, Barnes KC, Langefeld CD, Becker LC, Bowden DW, Becker DM, Chilton FH.
BMC Genet. 2011 May 20;12:50.

2. Genetic variants in the metabolism of omega-6 and omega-3 fatty acids: their role in the determination of nutritional requirements and chronic disease risk.
Simopoulos AP.
Exp Biol Med (Maywood). 2010 Jul;235(7):785-95.

3. A 'desaturase hypothesis' for atherosclerosis: Janus-faced enzymes in omega-6 and omega-3 polyunsaturated fatty acid metabolism.
Martinelli N, Consoli L, Olivieri O.
J Nutrigenet Nutrigenomics. 2009;2(3):129-39.

4. Apolipoprotein E polymorphism and fertility: a study in pre-industrial populations.
Corbo RM, Ulizzi L, Scacchi R, Martínez-Labarga C, De Stefano GF. Free PDF.
Mol Hum Reprod. 2004 Aug;10(8):617-20.

5. n-3 Fatty acid erythrocyte membrane content, APOE varepsilon4, and cognitive variation: an observational follow-up study in late adulthood. Free PDF. [This will be discussed later (someday). N-3 is a surrogate for mercury toxicity via fish/seafood consumption esp in apoE4 who hoard/harbor trace metals.]
Whalley LJ, Deary IJ, Starr JM, Wahle KW, Rance KA, Bourne VJ, Fox HC.
Am J Clin Nutr. 2008 Feb;87(2):449-54.

6. Moderate intake of myristic acid [MEDIUM CHAIN SATURATED FAT] in sn-2 position has beneficial lipidic effects and enhances DHA [OMEGA-3 PUFA] of cholesteryl esters in an interventional study [HUMAN].
Dabadie H, Peuchant E, Bernard M, LeRuyet P, Mendy F.
J Nutr Biochem. 2005 Jun;16(6):375-82.

7. Omega-3 fatty acid docosahexaenoic acid increases SorLA/LR11, a sorting protein with reduced expression in sporadic Alzheimer's disease (AD): relevance to AD prevention. Free PDF.
Ma QL, Teter B, Ubeda OJ, Morihara T, Dhoot D, Nyby MD, Tuck ML, Frautschy SA, Cole GM.
J Neurosci. 2007 Dec 26;27(52):14299-307.

8. Better memory and neural efficiency in young apolipoprotein E epsilon4 carriers. Free PDF.
Mondadori CR, de Quervain DJ, Buchmann A, Mustovic H, Wollmer MA, Schmidt CF, Boesiger P, Hock C, Nitsch RM, Papassotiropoulos A, Henke K.
Cereb Cortex. 2007 Aug;17(8):1934-47.

9. Superior performance [CHESS PLAYING/STRATEGIZING] and neural efficiency: the impact of intelligence and expertise.
Grabner RH, Neubauer AC, Stern E.
Brain Res Bull. 2006 Apr 28;69(4):422-39.

10. Evolution in health and medicine Sackler colloquium: Evolution of the human lifespan and diseases of aging: roles of infection, inflammation, and nutrition. Free PDF.
Finch CE.
Proc Natl Acad Sci U S A. 2010 Jan 26;107 Suppl 1:1718-24.

11. Accelerated evolution of nervous system genes in the origin of Homo sapiens. Free PDF.
Dorus S, Vallender EJ, Evans PD, Anderson JR, Gilbert SL, Mahowald M, Wyckoff GJ, Malcom CM, Lahn BT.
Cell. 2004 Dec 29;119(7):1027-40.

12. Apolipoprotein E: far more than a lipid transport protein. Free PDF.
Mahley RW, Rall SC Jr.
Annu Rev Genomics Hum Genet. 2000;1:507-37.

13. Meat-adaptive [URRG fat adaptive] genes and the evolution of slower aging in humans. Free PDF.
Finch CE, Stanford CB.
Q Rev Biol. 2004 Mar;79(1):3-50. Review.

Consciousness: The Great Leap Forward (Again?)

'Bigger Than The World'
Justin Timberlake

Collective Consciousness

There has been more discussions recently about collective consciousness just recently as we remembered global events that increased our awareness of our world, including 9/11. Actually part of the reason why I blog is because of 9/11. During the aftermath of the terror, heartbreak, and trauma that occurred in NYC, Pennsylvania and the Pentagon on that unforgettable day, there was a palpable change in country I felt. I don't know if it was collective but we all changed. I don't know if we were all connected at some point mentally, spiritually or noetically but somehow our consciousness appeared altered and irrevocably affected. For many months following the siege, the offices of the Wall Street Journal were displaced and journalists were spread out in outposts dispatching daily stories of immense hope, heroicism and triumphs of human spirit. It was difficult not to cry nearly everyday reading what ordinary people were doing endearing unimaginable pain and surviving extraordinary circumstances. Their unique, individual voices could not be missed or forgotten.



Conciousness Emerged 40,000 Years Ago

Intelligence, consciousness, and sentience. AWARENESS... Mmmh... the Matrix (nsfw) expanded my mind and awareness.

Scifi author Robert J. Sawyer wrote an essay in the anthology 'Taking the Red Pill: Science, Philosophy and Religion in The Matrix' entitled 'Artificial Intelligence, Science Fiction, and THE MATRIX'. Regarding humans, 'Intelligence is an emergent property of complex systems. We know that because that's exactly how it happened in us.'

'Anatomically modern humans -- Homo sapien sapiens -- emerged a hundred thousand years ago. Judging by their skulls, these guys had brains identical in size and shape to our own. And yet, for 60,000 years, those brains went along doing only the things nature needed them to do: enabling these early humans to survive.'

'And then, suddenly, 40,000 years ago, it happened: intelligence -- and consciouness itself -- emerged. Anthropologists call it "the Great Leap Forward."'

'Modern-looking human beings had been around for six hundred centuries by that point, but they had created no art, they didn't adorn their bodies with jewelry, and they didn't bury their dead with grave goods. But starting simultaneously 40,000 years ago, suddenly humans were painting beautiful pictures on cave walls, humans were wearing necklaces and bracelets, and humans were interring their loved ones with food and tools and other valuable objects that could only have been of use in a presumed afterlife.'

'Art, fashion, and religion all appeared simultaneously; truly, a great leap forward. intelligence, consciouness, sentience: it came into being, of its own accord, running on hardward that had evolved for other purposes. If it happened once, it might well happen again.'


Will A Different Conciousness Emerge Again?

Could we have another renaissance of culture, arts and technology? A neolithic intelligence, consciousness and sentience...?? I think we are on that path. The mind is the new frontier. Its barriers and miracles of its strength and potential power are being unlocked as we discover more (or learn from our ancestral warriors and healers)... Return to Matrix... energy begets energy. No energy is wasted. Life is sustained (Neo, kiss; Trinity, energetic voltage to the heart like an automated external defibrillator (AED).

Photo credit: themandus.com

Neanderthal Extinction

Neanderthals were far more advanced, culturally and technologically, and appreciative of consciouness more than earlier realized. An updated from Science Daily from today: Neanderthals More Advanced Than Previously Thought: They Innovated, Adapted Like Modern Humans, Research Shows. In terms of adaptation and evolution, the authors note 'Thousands of years ago, southern Italy experienced a shift in climate, becoming increasingly open and arid, said Riel-Salvatore. Neanderthals living there faced a stark choice of adapting or dying out. The evidence suggests they began using darts or arrows to hunt smaller game to supplement the increasingly scarce larger mammals they traditionally hunted. The fact that Neanderthals could adapt to new conditions and innovate shows they are culturally similar to us," he said.

The same speculation is discussed regarding recent information that grasslands were massively decreased as temperatures cooled at the end of the last Ice Age, approximately coinciding with the last days of the Neanderthals. Read Science Daily (August 18, 2010): Dwindling Green Pastures, Not Hunting, May Have Killed Off the Mammoth. As drier tundras replaced productive grasslands, large herbivorous mega-mammals like wooly mammoths, wooly rhinos and giant deer decreased in number. 'These habitat changes made grazing much more difficult for large mammals and dramatically reduced the amount of food available for them. The changes in grassland quality and availability coincided with increases in the distribution and abundance of modern man, Homo sapiens, ensuring a time of wide-scale upheaval for herbivorous mammals and other mammals that preyed on them.' (Photo courtesy, Science Daily)

Where did this leave the Neanderthals, the terrestrial carnivores (see post: Meat Made Us Smart, But Marine-based BAD*SSED)? Well. With considerably lower intakes of brain-nurturing omega-3 sources. Hunting smaller animals and increasing broad spectrum utilization of plant sources as the larger mammals migrated north away from Italian/Mediterranean and Euroasian shoresides toward Slavic and Siberian geographies.

Ancient man on the other hand continued to and perhaps were propelled toward marine-sourced carnivory and less plant based outsourcing as the mega-fauna dwindled in number and size. As brains improved synaptically, the bigger the brain, the bigger the hunt and the bigger the fish/seafood? It appears so from the evidence thus far.



Electrically, electrochemically, what is omega-3?

It fills in and controls our lipid double-layer cell membranes, and membranes are the master controllers in many emerging ways.

It behaves like high-speed internet. Long-chain Omega-3 fatty acids are the strongest, longest 'cables' in nature and behave like the cables of Comcast and DSL for our brain/heart/GI hardware and connections.




Bigger Omega-3 --> Bigger Brain --> Bigger Consciousness --> Bigger Display/Capture --> Bigger S*XXX --> Bigger Progeny/DNA-push-forward




References:

Explaining longevity of different animals: is membrane fatty acid composition the missing link?
Hulbert AJ.
Age (Dordr). 2008 Sep;30(2-3):89-97. Epub 2008 May 31.

Membrane fatty acids as pacemakers of animal metabolism.
Hulbert AJ.
Lipids. 2007 Sep;42(9):811-9. Epub 2007 Apr 27. Review.

Membrane phospholipid composition may contribute to exceptional longevity of the naked mole-rat (Heterocephalus glaber): a comparative study using shotgun lipidomics.
Mitchell TW, Buffenstein R, Hulbert AJ.
Exp Gerontol. 2007 Nov;42(11):1053-62.

The exceptional longevity of an egg-laying mammal, the short-beaked echidna (Tachyglossus aculeatus) is associated with peroxidation-resistant membrane composition.
Hulbert AJ, Beard LA, Grigg GC.
Exp Gerontol. 2008 Aug;43(8):729-33.

Meat Made Us Smart But... Marine-based, BAD*SSED

Meat Made Us Smart?

Making the evo/paleo blogs are the latest headlines... meat made us smart. NPR's article which is excellent: HERE. Love love LOVE NPR's new series. However. Meat. So what? I'm a carnivore and LUST4MEAT but my higher IQ is not attributed to meat. Figure from Richards et al PNAS 2000 and thank you to Stephan for the forward and rich insights HERE and HERE. Update: Richards et al later re-dated the Neanderthal bones to ~33-40 kya, not the stated ~28,500 yrs ago in the original article (Vindija 207 208 data).




Q: What Made Ancient Humans Rapidly DOMINATE the GLOBE?

A: Marine seafood (fauna and flora) including stems, leaves, tubers, berries, mollusks, crustaceans, fish, seals, dolphins, eels... and etc.




*** Summer Reading ***

Been doing some lightweight, softcore summer reading...
(a) MATT RIDLEY, 'Sex and the evolution of human nature: The Red Queen'
(b) 'Sex at dawn', authored by a psychologist and psychiatrist, C. Ryan and C. Jatha
(c) 'Carbs Can Kill!' by a pharmacist/physician, Dr. Robert Su MD, his personal account of complete health reversal (angina/CAD, skin issues, abdominal obesity, sleep apnea) from an MD point of view on a high saturated fat, carbohydrate-restricted (grain-free) diet. He is a fan of Feinman, Volek and the entire body of low-carb, high fat evidence, which he reviews in articulate and simple terms in his wonderful book. He interviews Sally Fallon author Nourishing Traditions (one of my favorite cookbooks) and WAPFer, HERE. Over 1100+ high sat fat, carb restricted cancer, disease and health references are listed conveniently on his site: HERE.

All 3 were extremely entertaining, enlightening and entirely edifying. Without really arguing the diet point, each of these scientific or sexual-psychosocial or medical/nutritional nonfiction are all for highly descriptive of a behavior or lifestyle written by evolution. (Thanks Dr. Dan for that motto!~) Unfortunately books #1 and #2 don't appear to understand the wild-human diet part... HHHhmmm.

Regarding Sex at dawn, like Melissa who reviewed it earlier HERE at hunt gather love, I agree the authors miss out on romantic love. Where is the LOVE??? Granted... lust does revolve the world around, but again, where's the *heart* sounds.

Also I believe in our human evolutionary history based on our close evo ties to ALL animals, including birds and fish... Ridley argues a better animalistic point that humans are somewhere in behavior (and the genetic studies appear to verify) between the birds and the bonobos/primates... Sexual dimorphism, behavior (mono- v. polygamous depending on fecundity of resources), courtship, songs, pair bonds + affairs, egalitarianism, child/egg rearing, paternity protection, etc. Elaborate shelter construction, prenatal and gestational nesting, omnivorous diet, etc-- Ridley forgot these factors, but I believe these are also common traits.


Biggest Organ

Surprisingly our largest organ which has made the most progressive advances over the last 25 million years... is the BRAIN. Cranial volume has tripled since primates branched off. Neanderthal brains were ~20% larger than current humans. Ancient human brains were also larger but by a smaller fraction, an estimated ~11% larger than currently. An MSNBC 2006 article discusses the microcephalin gene (D variant) which regulates brain size being found in both modern humans and Neanderthals, HERE. Does size matter? I believe so. Above diagram from Trinkaus Richards PNAS 2009, comparing isotope data between Neanderthals, ancient humans and related faunal assemblages.

Author Matt Ridley has tied together an eloquently argued subject that links sexual adaptation, success, survival with human intelligence.

[Smart? He is indeed smart. And funny as H*LL.]


Bigger brains lead to more food.

More food ---> More S*X

More S*X ---> More progeny and so on and so on

Food maybe a relative (Red Queen) euphemism...for any sustenance and nourishment (intellectual, emo, spiritual).




Obviously I've oversimplified and omitted the best thoughts.

Actually the beauty and clarity of Ridley's tight, dense, razor sharp scrutiny of all the lines of evidence and parallels drawn from the wealth of examples from the animal kingdom is how he scintillates the essence of human nature. 'Be different.'

Like a peacock's display, the brain's neurologic display (intelligence, humor, creativity, personality) is the point of attraction that he proposes was selected for over time. It's an interesting contention and makes insanely logical sense.

==>Recap: big brains-->big display-->big S*X-->big progeny





Ancient Humans: More Seafood (More S*X?)

Ridley discusses how bottle-nosed dolphins are perhaps the only other animal (mammal) with intelligence that rivals human intelligence and our complex language skills. However, dolphins brain:body ratios are only ~0.9% whereas humans are vastly higher ~2%. What do ancient humans have in common with our marine cousins, the social pack animal and s*xy/lusty predators, the dolphins?

Neanderthals were incredibly robust, hormonally superb specimens with excellent, dense, powerful bones, and complex communication for large mammal hunts and emerging culture 50-30,000 years ago. Shipman from PennState wrote in PNAS 2008 'Importantly, marine mammals, fish, and mollusks were systematically exploited by both Neanderthals and modern humans throughout the stratigraphic sequences at these caves.'

Above diagram, again, from Trinkaus Richards PNAS 2009. Obviously clear ancient humans were Marine Carnivores and Neanderthals were Herbivore Carnivores (?with possible broad spectrum sourcing including legumes and grasses).

Marine-sourced food is the most highest concentrated sources of omega-3 (marine veggies ALA, marine protein EPA DHA). Most fish or marine mammals don't produce it; THEY EAT IT. From sources concentrated up the food chain starting with algae and phytoplankton up the network, nitrogen and carbon atoms gradually change and can be measured a millenia later.


Omega-3 is BRAIN food.




We are what we eat: Stable 15N 13C Isotope Profiling

Right diagram, courtesy Prof White at Cornell for Geobiochemistry and stable isotopes in paleontology. Nitrogen concentrations up the food chain and marine food networks are laced with more complex hierarchy compared with terrestrial. Carbon is also concentrated up the food chain with again marine sources richer and with higher density carbon atoms compared with land-origin sources. Plants diversified and evolved during the early Miocene 25 mya from Calvin cycle only plants (C3) to more advanced plants that adapted to less water losses (via heat and/or via aridity) with an extra carbon altering step to malate (in the mesophyll vein) before entering the Calvin cycle (C4 plants). During cooling temps or droughts or fires that displaced lush forests and woodlands, grasslands, legumes and grains filled in then eventually flourished (C3 and C4 plants). See Left diagram.

As we can see from Prof White's diagram (right) that Neolithic Europeans who consumed less meat and seafood and more vegetables (C3, C4) had lower density 15N and 13C, compared with marine carnivores: (a) historic Eskimo hunter-gather-fishermen and (b) mesolithic Denmark people.

Go back and examine the 13C data (under 'Big Organ' or HERE) from Richards and Trinkaus PNAS 2009. C13 density is lower for Neanderthals compared with ancient humans yet about the same levels as other carnivores and omnivores (wolf, fox, respectively) and terrestrial small-large herbivores they were known to hunt and consume.

Data exists as early as 50,000 years ago, Neanderthals foraged small grain grasses, legumes and cereals in a small but non-neglible manner. See prior post.

Personally I think it is quite plausible that Neanderthals sourced their food in a very wide way that excluded much marine-based resouces, as indicated by the lack of density in the 15N and 13C isotope evidence.

Why?

I dunno.

Perhaps Neanderthals with their larger brains and early utilization of marine-based foods had a staggering boost in intelligence which translated to a more immense broad-spectrum resource utilization of legumes, small grains and cereals before ancient man got a clue (circa 12,000 years ago, neolithism).

Perhaps Neanderthals failed to figure out how to ferment and displace toxic legume and cereal-containing phytic acid? Ambient warm temperatures are required for fermentation. Perhaps this did not occur sufficiently (and/or by serendipity) until the last glacial maximum ended ~ 16 to 12,000 yrs ago as temperatures rose again finally.

Can a race over-innovate?

Can a race over-innovate to extinction? Esp when the other race is eating omega-3 fish oils by the ton having more s*x and more progeny?

Meat Science: Meat and Omega-3 as ACE-Inhibitors

T. Colin Campbell: No Longer Pied-Piper?

So... Again the data speaks volumes and the diminutive Ms. Mingers has put the final dagger in the vegetarian-low-sat-fat-fairy tale spun by so-called academic Campbell. The action is here: The China Study, My Response by Denise Minger.

You know if my teeth, eye color and health were ruined by a low saturated fat, low cholesterol, no meat, high soy, high grain vegetarian diet... I'd be mildly pissed.

And hungry...

For M-E-A-T . . . !



Meat Science

Added to NCBI PubMed in Feb, this newer journal features research and science in MEAT. I came across two articles here regarding protein from meat and beef which behave as ACE-inhibitors, one of the drugs deployed for hypertension, afterload reduction in heart failure and kidney protection in Type 1 (T1)and Type 2 diabetes (T2D) individuals. The mechanism of action of these drugs is blocking a pro-inflammatory-associated enzyme known as angiotension converting enzyme, ACE. Many peptides (proteins that are short sequences) are found in animal, seafood and plants that we consume that, in fact, have ACE-inhibitory action in mammalian systems. Even breastmilk contains lactoferrin which may inhibit ACE.

(1) A review of meat protein hydrolysates and hypertension.
Ahhmed AM, Muguruma M.
Meat Sci. 2010 Sep;86(1):110-8.

(2) Purification and identification of angiotensin converting enzyme inhibitory peptides from beef hydrolysates
A. Jang and M. Lee
Meat Science, Volume 69, Issue 4, Pages 653-661.


Clinical M-E-A-T Series *haa*:
o Meat as Medicine: Grassfed v. Conventional
o Phytanic Acid in Grassfed Meat: Binds PPAR-α and RXR (potent anti-inflammatory controls)


Other related meat science and research:
o Antihypertensive Activities of Peptides Derived from Porcine Skeletal Muscle Myosin in Spontaneously Hypertensive Rats
o Novel Angiotensin-Converting Enzyme (ACE) Inhibitory Peptides Derived from Boneless Chicken Leg Meat
o Antihypertensive effects and endothelial progenitor cell activation by intake of chicken collagen hydrolysate in pre- and mild-hypertension. [Endothelial progenitor cells are required for cellular and organ regeneration -- prior animal pharm Chicken Soup, Bone Marrow, and EPCs for organ regeneration]




Complex Chronic Diseases and ACE/AII Activity

Diseases since the DAWN OF TIME typically involve stress (physical, mental), trauma, infection, hormone imbalances, omega-3/omega-6 imbalances and elevated insulin, are associated with elevated ACE and AII activity. ACE is a membrane-bound peptidyl dipeptidase known to act on a variety of protein substrates in the extracellular space. Known functions are the formation of angiotensin II and the degradation of bradykinin. ACE has an indispensable role in animal physiology: aids in maintaining homeostasis and preventing death during duress activated by mammalian 'fight or flight', our hard-wired mechanism for survival. A sharp cascade of neuroendocrine and circulatory chemicals are released in stressful/imbalanced situations, as the body is trying to keep blood flow to the brain, heart and vital organs, heart pumping activity and other vital processes (see below diagram). ACE catalyzes the conversion from (less active) Angiotensin I to (more active) Angiotensin II. Do we require ACE and Angiotensin II? Of course, this system required to clear damaged tissue, maintain perfusion of tissues and organs and activate the immune system for healing after trauma and infection. Tourgeman discusses the role of Angiotension II here: ' (a) increases pressure within the kidneys, (b) increases fibrosis (scarring), (c) increases the recruitment of pro-inflammatory white blood cells, (d), increases the production of inflammatory cytokines (chemicals), and (e) increases cell proliferation.'

Courtesy RE Klabunde PhD Cardiovascular Pharmacology

Controlling Insulin, ACE and AII

Epinephrine (adrenaline), norepinephrine, cortisol, renin, aldosterone and other adrenal gland secretions are prompted acutely on a short-term basis. Under high insulin and chronic conditions, these powerful adrenal hormones and chemicals are inappropriately turned on long-term.

Any studies?

Frassetto et al (EJCN, 2009) showed that pre-hypertension normalized after 10 days on a hunter-gather paleolithic diet (grain-free, legume-free) in overweight men and women aged 18+ yo. This study was superby in reducing HOMA, insulin resistance, and basal insulin secretion by ~70%.

Subsequently, the systolic blood pressure reduced by 2.6 mmgHg (NS) diastolic blood pressure dropped from 71 by 3.1 mmHg (p=0.006); this is of huge magnitudes greater than those produced in the VAST MAJORITY of clinical anti-hypertensive drugs.

In younger patients the diastolic BP is more difficult to modify and lower; flips as we get older and arteries stiffen up.

A broad Cochrane review found "We found 92 trials that randomly assigned participants to take either an ACE inhibitor or an inert substance (placebo). These trials evaluated the blood pressure lowering ability of 14 different ACE inhibitors in 12 954 participants. The trials followed participants for approximately 6 weeks (though people are typically expected to take anti-hypertension drugs for the rest of their lives). The blood pressure lowering effect was modest. There was an 8-point reduction in the upper number that signifies the systolic pressure and a 5-point reduction in the lower number that signifies the diastolic pressure."

Again in the hunter-gatherer paleolithic diet (granted they were not yet hypertensive, but on the road there), IN ONLY DAYS of diet modification achieved statistically significant blood pressure reduction.

On this evolutionary/paleo diet, treatment participants consumed eggs, M-E-A-T, or seafood at EVERY MEAL.

Harmful?

No.

Healing.

And frequently and highly observed in individuals who lower their insulin levels and adopt an anti-inflammatory evo/paleo diet (and if necessary take antioxidants like omega-3, zinc, magnesium, etc).



Pharmaceuticals Do Not Work

IMHO ACE-inhibitor and ARB pharmaceuticals hardly at all or only marginally improve chronic disease processes. Unlike food components, drugs are strong. Artificial substances foreign to mammalian systems (xenobiotics) are not metabolized and eliminated in the same fashion as food components thereby potently binding and staying around quite a long duration. Besides binding one single receptor, they may inevitably activate or inhibit a vast variety of other interrelated receptor/enzyme systems. That is how we are built. Everything is INTERRELATED. Approximately 17% of users of an ACE-inhibitor report a dry, non-productive cough as a result of bradykinins building up which cause inflammation in the lungs, consequently resulting in an asthma-related cough. Captopril is the least because it does not affect bradykinin expression as much.

Dry, high-bradykinin, annoying, lingering, inflammation-related cough in affected ACE-inhibitor drug-users? Good? Probably not despite purported 'benefits'.

Another adverse effect of ACE-inhibitors (and ARBs) is hypotension (low BP), kidney failure and elevated potassium. These drugs, like all drugs, can cause what they are purported to 'protect'...

Blocking the final angiotensin at the receptor level is not good either. Recently angiotensin II receptor blockers (ARBs) are associated with a 20% relative increase in new cancer occurrence (7.2% v. 6.0%) compared with placebo in clinical trials (Sipahi et al, Lancet Oncology 2010). Lung cancer was the highest reported solid organ cancer incidence.

Food? Side effects? Generally not unless a food allergy exists to other food components or it promotes excessive insulin or blood glucoses or n-6/n-3 imbalances (e.g. starches, fruit, industrial farmed high n-6 meat/seafood).






Other Beneficial Foods Functioning as ACE-Inhibitors

Nutrigenomics is a new field that helps align our DNA expression to optimizing health via food, food components, and nutraceuticals (omega-3 fish oil supplements, vitamin D supplements, K2 supplements, magnesium, zinc, trace minerals, digestive enzymes, probiotics, etc). I discussed earlier: Nutrigenomics and Hypertension. The below list is adapted (I removed gluten #19).

Note: many of these are shore-based foods with high minerals (iodine, zinc, magnesium, selenium, manganese, chromium, etc).
1. Garlic
2. Seaweed
3. Tuna protein/muscle
4. Sardine protein/muscle (Anchovies too: Caeasar dressing)
5. Hawthorne berry
6. Bonito flakes (fish protein)
7. Pycnogenol (historical used flavonoid used as tea from pine bark)
8. Casein
9. Hydrolyzed Whey protein
10. Sour milk (fermented dairy)
11. Gelatin (protein)
12. Sake (fermented rice wine)
13. Omega-3 essential fatty acids -- even epigenetically reverses hypertension in bred rats
14. Chicken Egg Yolks
15. Zein (lysine and tryptophan-free protein from maize)
16. Dried Salted Fish
17. Fish sauce (fermented product)
18. Zinc
19. Rice bran (fatty acids, proteins)
20. Fermented cheeses
21. Tubers: potatoes, tumeric/curcumin, Japanese yams, Chinese yams,
22. Lactoferrin (human breastmilk, cow/goat/sheep dairy)
23. Cocoa storage protein
24. Pork protein/muscle
25. Chicken protein/muscle
26. Beef protein/muscle



Omega-3 Reverses Damage from Stressors (Insulin, Salt, Fructose, Cold Storage) and Epigenetically in Low-Protein-Mother and Stressed-Mother Rats

Omega-3 fish oil is just amazing stuff; it reduces ACE by more than one mechanism of action... It reverses all kinds of damage in rat studies and human studies caused by the S.A.D. and neolithic living. Unfortunately for the great majority of human trials, the research doses are often so low to be clinically inconsequential and inconclusive. For accurate results, I believe the dose needs to be calculated per person and based on (1) omega-3 deficiency and (2) accumulated omega-6 incorporation into cell membranes and adipose/fat stores. Current ratios in the U.S. of n-6/n-3 in blood or tissue membranes is 30:1 to (!!) 40+:1 and getting worse as we speak as many outspoken physicians, cardiologists and government agencies are trying to promote more high omega-6 canola oil and other oxidized refined vegetable oils to replace saturated fats.

Dietary n-3 PUFAs affect the blood pressure rise and cardiac impairments in a hyperinsulinemia rat model in vivo.
Rousseau D, Héliès-Toussaint C, Moreau D, Raederstorff D, Grynberg A.
Am J Physiol Heart Circ Physiol. 2003 Sep;285(3):H1294-302.

Interrelationships between salt and fish oil in stroke-prone spontaneously hypertensive rat.
Vaskonen T, Laakso J, Mervaala E, Sievi E, Karppanen H.
Blood Press. 1996 May;5(3):178-89.

Long-chain (n-3) polyunsaturated fatty acids prevent metabolic and vascular disorders in fructose-fed rats.
Robbez Masson V, Lucas A, Gueugneau AM, Macaire JP, Paul JL, Grynberg A, Rousseau D.
J Nutr. 2008 Oct;138(10):1915-22.

Beneficial effects of omega-3 fatty acid treatment on the recovery of cardiac function after cold storage of hyperlipidemic rats.
Ku K, Oku H, Kaneda T, Onoe M, Zhang Z.
Metabolism. 1999 Oct;48(10):1203-9.


Epigenetic implications:
Adult cardiorenal benefits from postnatal fish oil supplement in rat offspring of low-protein pregnancies.
Catta-Preta M, Oliveira DA, Mandarim-de-Lacerda CA, Aguila MB.
Life Sci. 2006 Dec 23;80(3):219-29.

Maternal fish oil supplementation benefits programmed offspring from rat dams fed low-protein diet.
Gregório BM, Souza-Mello V, Mandarim-de-Lacerda CA, Aguila MB.
Am J Obstet Gynecol. 2008 Jul;199(1):82.e1-7.

Developmental programming of renal glucocorticoid sensitivity and the renin-angiotensin system. [high omega-3 diet ameliorates high BP and high ACE activity in F1 generation born from rats given maternal-dexamethasone-dosing]
Wyrwoll CS, Mark PJ, Waddell BJ.
Hypertension. 2007 Sep;50(3):579-84. Free PDF.

The maternal diet during pregnancy programs altered expression of the glucocorticoid receptor and type 2 11beta-hydroxysteroid dehydrogenase: potential molecular mechanisms underlying the programming of hypertension in utero.
Bertram C, Trowern AR, Copin N, Jackson AA, Whorwood CB.
Endocrinology. 2001 Jul;142(7):2841-53.


Human study:
Fish oil [1.8 g EPA+DHA] prevents the adrenal activation elicited by mental stress in healthy [lean, young] men.
Delarue J, Matzinger O, Binnert C, Schneiter P, Chioléro R, Tappy L.
Diabetes Metab. 2003 Jun;29(3):289-95. Free PDF.

Insulin and Aging: How Paleo Works

Ai M showed the disparity between insulin changes between oral glucose loading (75 grams glucose) versus a high saturated fat CREAM dosing.


Carb equivalents 75 grams = 5 servings CARBs

Go to nutritiondata.com for more comparisons.

1 serv CARB = 15 grams

Dairy -- 1 cup milk = ~15 g

Fruit -- 2 bites is about 15 grams (small palm-full).

Grains (~ 15 grams):
Oatbran 1/3 cup. Oatmeal 1/3 cup. Bread 1 slice or half-slice depending on the density. Rice 1/3 cup. Pasta 1/3 cup. Broccoli 2-3 cups just kidding but infinitely more compared with grains which have an insanely high-carb density as well as genetic propensity to trigger stress, glucocorticoid and the expression of other 'bad' genes. See prior animal pharm FUNGENUT post HERE.

Legumes (~15 grams):
1/2 cup beans


Ai M et al. Clinica Chimica Acta 387 (2008) 36–41. Email me for the PDF if desired.

What is PALEO?
None of the above
--no dairy (except casein-free clarified butter/GHEE or whey protein)
--no grains (corn, oats, gluten (wheat/barley/rye), rice, etc)
--no legumes (beans, soybeans (unlesss soaked+fermented), peanuts)


Please see recent NephroPal post:
Insulin and Aging: How Paleo Works

Click above link...

Cardio Controversies: Tale of Two Equal LDLs and 17-fold MI Risk

Figure 2. Cox proportional hazards survival curves demonstrating
time to acute MI for patients with a yearly calcium volume
score change > 15% or < 15%. Callister et al, 2004 ATVB.

TITLE: Progression of coronary artery calcium and risk of first myocardial infarction in patients receiving cholesterol-lowering therapy.

Free PDF click HERE. Raggi P, Callister TQ, Shaw LJ. Arterioscler Thromb Vasc Biol. 2004 Jul;24(7):1272-7.

OBJECTIVE: Statins reduce cardiovascular risk and slow progression of coronary artery calcium (CAC). We investigated whether CAC progression and low-density lipoprotein (LDL) reduction have a complementary prognostic impact.

METHODS AND RESULTS: We measured the change in CAC in 495 asymptomatic subjects submitted to sequential electron-beam tomography (EBT) scanning. Statins were started after the initial EBT scan. Myocardial infarction (MI) was recorded in 41 subjects during a follow-up of 3.2+/-0.7 years. Mean LDL level did not differ between groups (118+/-25 mg/dL versus 122+/-30 mg/dL, MI versus no MI). On average, MI subjects demonstrated a CAC change of 42%+/-23% yearly; event-free subjects showed a 17%+/-25% yearly change (P=0.0001). Relative risk of having an MI in the presence of CAC progression was 17.2-fold (95% CI: 4.1 to 71.2) higher than without CAC progression (P<0.0001). In a Cox proportional hazard model, the follow-up score (p=0.034) as well as a score change >15% per year (P<0.001) were independent predictors of time to MI.

CONCLUSIONS: Progression of CAC was significantly greater in patients receiving statins who had an MI compared with event-free subjects despite similar LDL control. Continued expansion of CAC may indicate failure of some patients to benefit from statin therapy and an increased risk of having cardiovascular events.
PMID: 15059806



Cardio Controversies: Dr. Callister MD

I think Callister is cool. First he found statins were associated with regressed EBCT scores in 1998 but then confessed up when he could not replicate it in several subsequent trials. He has even postulated why. Correctly I think!

He and his colleagues have found a dilemma in current cardiology concepts, much like Dr. Superko. Despite LDL < 120 mg/dl and treatment with statins, patients progressed to an MI when the calcium volume score via EBCT increased > 15% annualized. In fact, they summarize that "the relative risk of suffering a MI in the presence of CVS progression was 17.2-fold (95% CI4.1 to 71.2) higher than that of subjects without progression (P<0.0001)."

Our goal at TYP as designated by Dr. Davis from his extensive experience and research is for EBCT annualized progression of no more than 10% to halt all risk of long-term clinical CAD events. Naturally, some EBCT regression is desirable.



Is LDL Reduction Necessary?

For reduction in hard clinical events, is LDL reduction really necessary? Actually, I don't think so... From lipid researchers like Dr. Barry Sears PhD on omega-3 and the tremendous outcomes from the secondary prevention Lyon Heart Diet trial, we know that with a significant reduction of dietary omega-6 toxic vegetable oils and sufficient increments of dietary omega-3 (ALA, EPA, DHA), clinical CAD events can be nearly halted in very high risk group of CAD individuals. Moreover, with only minor improvements in the n-6:3 balance a reduction in all-cause mortality (cancer, suicides, accidents, etc) in addition to CAD mortality and events was observed in this landmark study. Recall, these improvements were witnessed with no improvements in total HDL (final 49 mg/dl) or LDL (final 161 mg/dl). I always have to ask why save the heart and coronary vessels yet advance to experience cancer and/or suicide and depression? One of the most tragic and saddest stories that I have come across related to the low-saturated fat debacle is that of the famous Dr. Pritikin who conquered heart disease but committed suicide after silently battling leukemia. What was he missing? Could his demise have been prevented?



Low Dietary Saturated Fat

Why may low saturated fat be dangerous for the long-term? Can a 'deficiency' in dietary saturated fat be as insiduous and quietly dangerous as cancer or subclinical atherosclerosis itself?

I see a lot of HDLs in the 20s 30s 40s (or HDL2b nonexistent to single-digit). What is wrong with these kind of numbers? For one, according to clinical trials, they are highly associated with CAC progression and early events. Of course, there are cases that are exceptions to the rule... for instance if you are . . .
(1) Nissen infusing HDL-apoAI-recombinant pieces into your arm every night (JUST KIDDING... don't get any stupid ideas)
(2) an apo A1-Milano carrier
(3) allergic to kryptonite *haa*
(4) consuming boatloads of niacin or omega-3 fish oil until gills grow


Are low HDLs a sign of dietary saturated fat deficiency? Or just high carbohydate intake? Or both? Moreno JA et al showed that with a high fat diet (40%) both high saturated fat (20% SFA) and high monounsaturated fat (22% MUFA), shifted individuals equally from pattern B to A when compared to a high carbohydrate (CHO 57%) diet (J Nutr. 2004 Oct;134(10):2517-22). PDF click HERE. However, like other saturated fat studies, only the SFA diet across every apo E type (4/3, 3/3, 3/2) raised the HDL to the highest degree. Interestingly, apo-AI was increased as well to the greatest magnitude with the high saturated fat diet and was the case for every apo E genotype. Both HDL and apo-AI are atheroprotective and associated with plaque regression. See below chart (p<0.05). FYI, these diets in healthy volunteers were still very VERY high carbohydrate at (yikes) 47% and explains why a higher majority of individuals were pattern B (predominance of small dense atherogenic LDL) to begin with, particularly in the males. Certainly, I know I would immediately be clinically T2DM with this type of diet.





Callister's Other Findings: 'Incomplete Effectiveness of Statins'

Callister et al concluded that 'statin resistance' may be responsible for the lack of efficacy for these drugs in preventing hard clinical events observed in this trial. How about...

Lack of HDLs?

Excessive carbohydrates? 47+% Carbohydrates in the AHA 'low fat' diet?

Lack of dietary saturated fatty acids?

The authors concluded that "molecular mechanisms—as yet not fully understood—could help explain the incomplete effectiveness of statins therapy. The HMG-CoA reductase enzyme is a pivotal rate-limiting enzyme in the production of intracellular cholesterol and is selectively inhibited by statins. To inhibit excess synthesis of cholesterol, the HMG-CoA reductase enzyme is degraded in the presence of high levels of intracellular mevalonate and sterols. Statin resistance at the cellular level has been described to occur via 2 mechanisms: overexpression of the gene regulating secretion of the HMGCoA reductase enzyme and loss of degrading ability of the enzyme in cell cultures exposed to high concentration of lipoproteins and lovastatin in the medium."


OK... well they were close. HMGCoA reductase is certainly controlled by several factors. Ness and Chamber discuss this 'cholesterol buffering capacity' effect of HMGCoA reductase, the enzyme that produces LDL-Cholesterol (the good lbLDL and the 'bad' sdLDL) and is mechanistically inhibited by statins. Unfortunately like all interconnected systems in biological environments, feedback control ultimately inhibits or stimulates HMGCoA reductase activity based on many factors which are regulated by needs for growth, reproduction, fasting v. fat-storage, and relaxation. Click HERE.
--dietary cholesterol downregulates (yup... cheap-egg-yolks vs. Crestor; yolks WIN)
--hyperinsulinemia turns it on (poor glycemic diabetic control, high-carbs-low-fat-idiocy, again)
--hypothyroidism turns on
--peri- and menopause (low estrogen states -- or like those induced by $*%&@# contraceptives and $*%&^! progestins)
--high cortisol (mental stress, physical stress)
--lack of bile salts (taurine deficiency)




Factors NOT Affected by Statins: Lp(a), IDL, Small LDL, Microbes

Callister and the other authors are brilliant! In addition, they concluded: "Because we did not measure hemoglobin-A1c, we were unable to verify whether the glycemic control had an effect on CVS progression and development of MI. Lipoproteins not affected—or incompletely affected by therapy with statins—such as Lp(a), small dense LDL, and other mediators of vascular damage (viruses, homocysteine, fibrinogen, Chlamydia Pneumoniae, and others) may also have played an important role that could not have been detected because of the design of our study."



What Does Lower Lp(a), IDL, Small Dense LDL and Microbial Burden?

Oh please... Gentle Readers... I hope you get this correct.

Yes?

Saturated fatty acids, my dear audience members, of course.

Synergistically with a low LOW carbohydrate diet (or no carb).

Did you know that coconut oil, grassfed ghee/butter, cream, tallow, lard (which contain short-, medium- and long-chained saturated fatty acids) control and kill yeast, parasites and other microbes like Giardia, Salmonella and Campylobacter, in vivo and in vitro?



Krauss is in the House! The Three Axes of Evil

Yes -- of course (without Superko's help) Krauss has figured it out again and confirm the theories above as well as what we already acknowledge and tackle at TrackYourPlaque. Subfraction of lipoproteins yields the 'death' bands on ion mobility analysis which are independent subsets of cardiovascular risk. (Krauss et al, Arterioscler Thromb Vasc Biol. 2009 Sep 3. Not free yet.)

(PC1) LDL-associated risk: Concentration-sdLDL, Small Dense LDL, VLDL [Lipoprotein (a)]

(PC2) Metabolic Syndrome/Hyperinsulinemia pattern of decreased large HDL, increased small/medium LDL, and increased triglycerides (eg, Pattern B)

(PC3) HDL-associated protection: large HDL subfraction ('absent' band)

Note: Krauss does not list Large LDL-P as one of the axes of coronary risk. After reviewing 3 large landmark trials, he and the other researchers concluded Large LDL are not associated independently with CAD risk. Again, the presence of small LDL-IVb (the densest of 7 subparticles) is associated with risk and progression of plaque, not a high particle count of Large LDL.

Krauss and the other authors state, "Our study demonstrated that (1) levels of small/medium LDL particles are associated with [CV disease] and (2) levels of large LDL particles are not significantly related to cardiovascular disease, is consistent with other large prospective cohort studies whose data were obtained by 2 different lipoprotein measurement techniques: the Quebec Cardiovascular Study (GGE) and the Multi-Ethnic Study of Atherosclerosis and Women's Health Study (NMR). (p. 5)"

Large-LDL are Not Associated with Increased CAD Risk

This bears redundancy. Many cardiologists and even NMR experts do not understand this concept. Repeat... Krauss and other cardiologists found no increased risk associated independently with the presence of Large LDL.

Why is Large LDL even implicated sometimes?

Are fire-fighters implicated in causing atrocious out-of-control fires?

No. That is frankly ridiculous...

The arsonist is the smallest densest LDL. (See PC1 or PC2.)
And, the co-conspirator is the lack of large HDL2. (See PC3 or PC2)


(Read: dietary saturated fat deficiency. Excessive compliance with the AHA low chol/sat fat indictment).

Genetically we are all different -- some individuals naturally produce more Large LDL (apo E4? these folks elude infectious agents better, esp coupled with Lp(a); unfortunately the CAD is concordantly worse on inappropriate diets, e.g. non-ketogenic). However, when the NMR is examined, these individuals who have both CAD and bunches of Large LDL exhibit the 'death' band. Subfraction particles of LDL-IVb will often be 10x higher than normal. Or even 20x higher. What's normal and optimal? Optimal is none to 0.60% in my opinion.




Pattern A + the tiny LDL-IVb 'death' band is not a good thing.

You only need one axis of 'evil' for heart disease and EBCT progression.

Paleo folks sometimes have very high LDL mass and stunningly enormous proportions of Large LDL. Funny... this is also observed in individuals in longevity and centenarian studies. The long-living 100-year old Ashkenazi Jewish (pro-bands) have enormous HDL and Large LDL yet the small dense LDL was minor consisting of ~6-7%. Is all that Large LDL harmful? I doubt it. Their offspring have HDLs like us mod-high fat Paleo folks of 80s-100s. Okinawan centenarians also have enormous HDL of 60s with consuming goat milk full of saturated fat (MCTs), lard, fatty pork and gamey goat sashimi. Their LDLs are high in the 100-120s mg/dl like the Ashkenazi.

Read here: Benefits of High-Saturated Fat Diets (Part II).

For the Paleo/Primal/PP folks, if the LDL is mostly (or all) large, no problem. If however there are some of the smallest densest stuff (subspecies: LDL-IVb, the black sheep) and no large HDL2, then... it... maybe a problem. LDL-IVb is eradicated within 4wks with the right diet. Low low carb, fat and protein, Paleo.

Only subfractionation of the lipoproteins will identify the culprit.





Statins Fail to Improve ALL 3 Principal Components (PC)

Do statins help with any other of the above independent axes of coronary risk: PC1, PC2, or PC3? Or other identified CAD risk factors: vitamin D deficiency? Omega-3 deficiency? Hypothyroidism? Excessive omega-6 clogging up cell membranes and raising serum insulin and inflammatory markers?

Well... statins raise vitamin D. (yeah... Sunshine/ supplement v. Crestor which raises vit D 159%? Sun+Vitamin D WIN. When my blood [25OHD] increased from 20 to 70 ng/ml (350%), my HDL increased 29%. OK... here is a vitamin D formula: every 10% vitamin D conc increase = 1% HDL increase; according to Castelli, every 1% HDL increase is equivalent to 2-3% CAD relative risk reduction)


Well...statins may raise HDL max 5-15% yet niacin raises HDL 30-200% (depending on duration and patient population).

So the action on promoting regression via HDL by Niacin is 2 to 40x more than statins.

Niacin prominently lowers Lp(a), small dense LDL/IDL, triglycerides and provokes shifts to Pattern A. In the HATS trial, recall, after 3 yrs, niacin raised HDL 30% and HDL2 60%. Niacin was associated also with reductions in blood pressure. Statins are not in any trial.

In fact, any non-synthetic, therapeutic intervention that raises HDLs also lowers Lp(a), IDL, small dense LDL/medium LDL and triglycerides. And increases nice large buoyant LDL. Indeed, these lipoprotein species all improve in parallel. Conversely, they are exacerbated in parallel. With no exception, any strategy that raises HDLs consequently affects blood pressures positively downstream (eg, carb restriction, body fat loss, lean muscle gain, yoga, omega-3, vitamin D, saturated fat intake, thyroid replenishment, hormone optimization, many antioxidants and proanthocyanidins).

Except statins. What the authors missed mentioning was that in addition to 'statin resistance', statins worsen Lp(a) and Percent-sdLDL. And they fail to shift to pattern A. What else?
Statins s*ck.



Correctly Catching the Calcification Culprit(s)

TrackYourPlaque is a self-management program. To optimize the program and control plaque, one must accurately and knowledgeably assess personal and familial risk factors that caused suboptimal lipoproteins and/or positive EBCT scores and progression. The three factors listed above comprise 99% of the most common coronary culprits.

If one is just trying to beat down the LDL-Particle Count into submission and fails to take into account the three 'axes' of coronary risk, one will invariably miss the big picture.

Is it... dangerous...??

Certainly... it is not equivalent to EBCT stabilization or regression. Targeting and ameliorating the correct coronary culprits on the other hand yields potent control on plaque and reduce EBCT calcification progression to < 10%. For regression in 9-18 months on EBCT, 'perfect' lipoproteins are not mandatory but a trend toward improvements in both reductions in small dense LDL, IDL, Lp(a) and increases in HDL2 and relative LDL-buoyancy are requirements. Control of hypertension, more vitality, loss of body fat are all extra side perks.

Do you have 'leaky gut' where microbes are flowing into the blood stream from the intestines?
Do you have low HDL?
Do you have high small-LDL?
Do you have Pattern B?
Do you have Lp(a) and/or high homocysteine?
Do you have progression or calcium score > 10% annualized?
Do you have premature CAD or stroke or peripheral vascular disease or renoarteriosclerosis in your family history?
Do you have proteinuria, dialysis or chronic kidney disease in your family?
Do you have heart failure in your family history?
Do you have 'statin resistance'?

Then... one cannot hesitate or prolong an approach that is more targeted and aggressive than the one that Callister and his colleagues discussed ('incomplete effectiveness') associated with a 17.2-fold MI-risk in 6-7 years.


Ketosis/niacin, low LOW carb Paleo diets, mod-high SFA diets, high omega-3 supplementation, dietary omega-6 elimination, hormone optimization, cardio/weights and many MANY other TrackYourPlaque strategies improve all three axes of high cardiovascular risk.



Related posts:

Egg Yolks and High SFA Diet Raise HDL2, Lower IDL VLDL triglycerides, and Increase LDL Particle Buoyancy

Benefits of High-Saturated Fat Diets (Part I): Krauss 18%-High SFA Diet Lowers sdLDL particularly LDL-IVb, Raises HDL2b and lowers IDL VLDL triglyerides

Benefits of High-Saturated Fat Diets (Part III): High SFA, Low Carb Paleo Diet annihilate sdLDL from 1000nmol/L to nearly no particles or 'None', Raises both HDL2/HDLs 200-400%, Lowers IDL VLDL triglyerides, Lowers Lp(a)

HDL2b: Quintessential Regression Particle and How to Raise It

Lp(a) and Women's Heart Risk

Umbellularia Californication: SFA kicks olive oil's *ss

Lp(a) and the Power of Fish Oil (8.5 grams/d EPA DHA)