Wednesday, April 09, 2014

Dr Doug Wallace on mitochondria



This link came to me from Bill Lagakos via Facebook. It covers a lot of ground and is, unavoidably, a little superficial in places when the subject matter is very deep. He mentions his work with mice made heteroplasmic for two different strains of mitochondria, the NZB and the 129. Both work perfectly well as the sole mitochondrial population giving normal mice. Engineering heteroplasmy produces mice with a stack of problems in high energy demand tissues.

I got to this point, about half way through the presentation, before the penny dropped that the speaker was Doug Wallace, group leader of the people who published this paper

There is a more detailed analysis of this aspect in Nick Lane’s comment in the same edition of Cell about why heteroplasmy might be a Bad Thing, especially in high ATP demanding cells.

I spent much of the presentation thinking that there was no mention of nutritional tools for managing mitochondrial heteroplasmy and very little about mitochondrial mutations and ageing but these came up in the Q and As at the end. The nicest question was about intermittent fasting but Wallace immediately threw in a ketogenic diet as a potential technique for clearing out deleterious heteroplasmic mitochondrial sub populations. He also mentioned the ubiquity of low level heteroplasmy and pre ovulatory selection for optimal mitochondrial population in oocytes...

A lot of ground. Much there which makes sense.

Peter

54 comments:

Puddleg said...

You might like this:
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0092887

These data provide the first direct evidence supporting mitochondrial dysfunction in Gulf War illness. Findings merit replication in a larger study and/or corroboration with additional mitochondrial assessment tools.

Having seen NZ army rations, with bags of sugar and no real fats, it wouldn't surprise me if a lot of problems faced by soldiers today are made worse by metabolic diseases as well as toxic environments and chronic stress.

callingnew said...
This comment has been removed by the author.
callingnew said...

fascinating presentation.

here's an interesting article exploring the role of propionic acid in autism and other conditions.

AUTISM: METABOLISM, MITOCHONDRIA, AND THE MICROBIOME

http://www.gahmj.com/doi/pdf/10.7453/gahmj.2013.089

Peter said...

Ta callingnew and George.

Go the d in to the label too.

Peter

Al Towers said...

He gave almost this exact lecture (probably exactly, the title is the same but I can't speak for all the data, haven't watched the whole video yet) at my university in the fall, I thought it was probably the best seminar I had ever been to, but there wasn't that many people in attendance, surprisingly. At that presentation someone asked specifically about ketogenic diets, and, if I remember correctly, he said that due to the high chance of adverse effects in certain populations it was probably best to avoid them altogether as a therapy.

Peter said...

Al, That's interesting. I wonder what the population base is for adverse effects for ketogenic diets might be. I do wonder about tropical starchivores. Catastrophic effects of ketogenic diets in children can probably be traced to basing them on corn oil and/or safflower oil. Some of the infant formulations in the Freedman book are pretty scary re PUFA.

Perhaps that's why the questioner asked about intermittent fasting rather than ketogenic dieting! Or perhaps Wallace was thinking about LCHAD deficiency or MCAD deficiency... But then fasting is pretty risky in these patients too.

Peter

Peter said...

Wallace cites Schon and ketones for severe heteroplasmic diseases (in cell culture). This looks like the work:

http://www.ncbi.nlm.nih.gov/pubmed/15389892

Interesting.

Peter

Unknown said...

Bill got that link from me, I believe Petro. Gene expression levels and covalent modification of biomolecules are just two types of biochemical responses that lead to cellular heterogeneity. The key point missed in this disscusion is that Wallace is telling biology that the mitochondrial wiring diagram meshes the cell membrane voltage to the inner mitochondrial membrane. Centanarians have a lot of heteroplasy. This implies it is good, when you have a surface understanding. Lane makes the key point of differentiation. Cells with high ATP potentials do poor with heteroplasmy? Why is that fundamentally Petro? It is a thermodynamic problem in mass equivalence. It is not a biologic process it is a quantum one. Wallace is saying this loud and clear, but biology folks do not understand what he is really implying. Biology does not understand mass equivalence link to bioenergenics yet. Those changes in energy may trigger variations in pathogenic steps in cancer, viral infection (George) or variable drug responsiveness in diseases. Mitochondria are organized according to the statistical nature of the Second Law of Thermodynamics, and as such, it deals directly with the mass equivalence relationships of energy. This is fundamentally why apoptosis and autophagy are directly linked to cell volumes and mass. Moreover, in physics Feynman said time is a direct function of mass. This directly links mass to telomere lengths in biology. Ketosis decrease heteroplasmy because it provides the best source of subatomic particles with a "massless source of energy" making the cell volume and mass smaller. This is why laminin defects kill people with progeria and why kids with CFTR defects in CF die. Cells lose their tensegrity. Protons have a mass, and electrons do not. I am waiting for you to realize this. And as such this is why mitochondria pump them out and use them as signaling particles. We use electrons for something else. Complexity. Our most complex tissues are built around free electrons and photons. The human brain being case example. The more protons you make, while simultaneously having less electrons, means the cell volume increases and complexity in signaling drops.......what organizes it all? The redox potential in cell membranes and mitochondria. What links them all together? This is the wiring diagram Wallace is connecting in his mind on his slide. In Wallace's diagram, the wiring is in the middle of the 'anatomy part' of a cell and the 'mitochondria part' of the cell. When a cell’s mass/volume is higher it is less energy, and in a thermodynamic unfavorable state. Efficiency is lost across the whole cell over time because it must lose's more energy back to the environment than it can retain, so it swells. This is why mitochondrial change (heteroplasmy) happens faster as volumes or mass increases in a cell. ATP dependent cells swells much faster than ones who are using ketosis. Ketotic cells shrink much faster. This is why biology organizes its 'change programs' around autophagy and apoptosis. This is where heteroplasmy becomes hugely beneficial with respect to the energy mass equivalence relationships. When a cell gets larger it activates autophagy and apoptosis programs and cell death comes faster and it depletes stems cells. Mitochondria swells it induces either cell suicide or heteroplasmy. Heteroplasmy is a solution to a bas environmental problem. If you can overcome it, your end result as a centenarian will be a lot of heteroplasmy because it is proof of ultimate adaptability in the face of environmental change. When cells or mitochondria swell and do not have an outcard, so to speak, stems cells are depleted death comes. Protons have mass, energy and info. Electrons have energy and information without mass. This is why ketosis is an electron story.

Stuart said...

Here is the exception..25% of the population in NA
http://blog.trackyourplaque.com/2011/07/the-exception-to-low-carb.html

LeenaS said...

To heartlifetalk:
By now I know even personally several ApoE types that are doing remarkably well on LCHF. It really does not seem to be the cholesterol...

Peter said...

Jack, I'm still plodding one step at a time.

Heartlifetalk, Interesting. I've always struggled with Dr Davis' saturophobia. Ten years ago it was across the board and quite embarrassing to read, so I stopped. Nice to see it's limited to apoE4 folks now. I note the data are "sketchy". Let's see what happens to that last 25% over the next ten years...

Peter

Peter said...

George, there was a report in the press here that the main drugs of abuse in UK troops in Afganistan are anabolic steroids. You can possibly be a peak level athlete in combat on sucrose but I guess it's bloody hard work. You need to maintain muscle mass when your life depends on your performance in a real life "gym".

The thought of 'roid rage in military personel. Gulp.........

Peter

Anonymous said...

I'm happy to report back in 8 years time re the e4/e4. I'm generous like that.

Of course it may simply be a race between CVD, AD and the many idiot drivers on the roads as to who gets me first.

In the interim, I'll resist the urge to go vegan. Ta.

Spunk said...

Leena have those done advanced testing from say HDLabs and found their risk factors reduced?
Every case except one E3/4 who had thyroid med correction are not able to tolerate high fat diets as most are hyper absorbers of fat with delayed ldl clearance genetic deficits and I have been observing at Dr Davis Trackyourplaque.com for me than a few years and proved it for myself.
Now being a vegan just because of this is just as extreme as eating 70% fat.
Now what is the reason for the professor being reluctant to apply it to the population?
http://www.prescription2000.com/Interview-Transcripts/2011-03-10-joe-d-goldstrich-integrative-cardiology-transcript.html

Spunk said...

JKruse totally new simplistic theory you need a research lab if you can get one so we will get a story like below that is understandable.

http://www.eurekalert.org/pub_releases/2014-04/sri-tsd040414.php

Peter said...

Spunk,

You need to add some punctuation.

Peter

LeenaS said...

@Spunk
At least one of them has, and they were ok
... and btw, she looks at least 10 years junior to others of her age.

Then again, in Northern Europe LCHF may be easier to do right, since good quality local butter, tallow and broths are all available?

Stuart said...

Leena if they are in Europe I doubt that advanced testing is done there.
There is a large group of E4 over the years that have not responded well to high fat. The mechanism is that high fat generates high post prandrial tryglcerates. If get a hold of a CardioChek home meter and trig strips and tries a fat challenge test by consuming a large amount of fat the reading will much higher than normal. Unfortunately this is a well known fact among even heart specialists. There even is an E3/4 member there who discovers people experimenting with high fat diets and putting their data say from a nmr test on the web and post about it as a lesson to others. Dr Davis's has subscription fee for his forum so this information is not more widely known. This has not been known for sometime.

Berkley guide
http://www.bhlinc.com/clinicians/test-descriptions/ApoE

Here is the Genova guide
http://www.google.ca/url?sa=t&rct=j&q=&esrc=s&source=web&cd=3&cad=rja&uact=8&ved=0CDYQFjAC&url=http%3A%2F%2Fwww.gdx.net%2Fcore%2Finterpretive-guides%2FCVHealth-Genomic-Interp-Guide.pdf&ei=mp9IU8f9FsnPsATX54DABQ&usg=AFQjCNHvZdgK9FIIcEpmKLGS1Wbqm1xssg&bvm=bv.64542518,d.cWc

Stuart said...

meant to say this has been known for some time but not widely known as 20 years of data and these reports are not widely read although the research has been out there. There is more to back this up. excuse the slips as its late here and I don't write too good.

Peter said...

heartlifetalk,

Your citations are lost in the lipid hypothesis. You are using guidelines which look at lipids and associate those lipids with CVD risk. You have a basic assumption that blood lipids cause CVD. You will make many wrong choices based on this hypothesis. From your second citation “ Total- and
LDL-cholesterol concentrations increase in a step-wise fashion with sum of the APOE alleles (E2/2 < 2/3 < 2/4 < 3/3 < 4/3 < 4/4)”.

You are in the wrong place on the net to cite TC and LDL as risk factors for CVD.

FYI CVD is caused by purple spotted LDL®, which is made of hyperglycaemia.

Peter

Anonymous said...

Peter, I found this reference on the blog of retired anesthesiologist Dr. Gerald Davis.

17. Wallace, Douglas C. A Mitochondrial Paradigm of Metabolic and Degenerative Diseases, Aging and Cancer: A Dawn for Evolutionary Medicine. s.l. : Annu Rev Genet 2005: 39: 359.

http://preventionnutrition.com/lessons-from-100-years-of-ketogenic-diets/

http://preventionnutrition.com/about/

He's also in the UK.

Cheers,

Melchior.

Anonymous said...

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821041/

Spunk said...

"You have a basic assumption that blood lipids cause CVD."

No it is one contributing risk factor. There are even some rare ApO-3/3's who also have this fat absorption problem and one recently reported improved results not based exclusively on lipids. I have seen it in myself as I tried moderately higher fat diet.
Yes these companies are involved in lipid testing among other things. Dr Thomas Dayspring of HDLabs in one case study recommended lowering fat consumption and increasing carbs.
I think Lara explains it best
http://www.lmreview.com/articles/view/omega-3s-apoe-genotype-and-cognitive-decline/
I think now the gut biodome has a influence in this defect and seems negative for a LCHF approach.
Enjoy your blog and comments section.

Peter said...

Thanks Melchior, there's a lot of background there!

Peter

Kindke said...

Peter I thought you might be interested in this paper...

http://www.ncbi.nlm.nih.gov/pubmed/20682684

In particular,supplementary Fig. 4E, which shows much lower oxygen consumption in adipocytes from obese people when mixed with the uncoupler FCCP.

Given this is all done in vitro from cells grown from pre-adipocytes I cant for the life of me think of any explanation for this.

fat burning and energy wasting within the adipocyte seems to be a key aspect of a lean and healthy metabolic profile.

Sabine said...

Regarding APO E4:
It may be even more important for carriers of APO E4 to eat very low carbohydrate and high fat. It may also be important for them to have higher cholesterol.

Chris Masterjohn and others have been writing about this: http://www.cholesterol-and-health.com/Cause-Of-Alzheimers.html

Similar effects will be at work in other cells of the body.

Somewhere in his paper he concludes: "It may well be that apoE4 is only a harmful gene if it is accompanied by a high-carbohydrate diet ...."

Ken said...

Peter, thanks for post. Have listened to other lectures by Wallace with much interest.

Here is a link that might interest you --

http://www.ncbi.nlm.nih.gov/pubmed/24652947

, published within last month. It looks possibly important to my much less well trained eye and I think does not require any more introduction. I have only looked at the abstract.

raphi said...

Excellent video lecture, really appreciated it!

Peter, could you expand on the final question/comment psoed by the audience member @ 1h07:37?

It was something like "Deleterious (mtDNA?) alleles in mice are progressively less in every generation - but not in humans." Why? How does that impact the 'leaky wiring' theory...?

Dr.Kruse -Although quantum physics ultimately underlies electron & proton behavior in any system, what Wallace is proposing still **seems** explicable with classical physics for its basic premise.....right?

Unknown said...

raphi Wallace is introducing modern biology to electrons which are masslass energy and information. Peter is finding protons interesting, which are masses with energy and info......Einstein's mass equivalence equation tells you why life organized around what it did.....the redox potential. Electrons = a high redox potential and excess protons lower it.

Unknown said...

Raphi realize that Wallace and Heteroplasmy = excessive protons = more mass = more energy loss = less electrons.

Both mitochondria change programs are tied to cell volumes and sizes......autophagy and apoptosis

Unknown said...

Peter here is a boost or push for your proton series.......for you to ruminate on later. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0093065
PHYSICS GEEKS AND INTERESTED BIOLOGY GEEKS: electrons differ in 2 respects: energy and spin. Life’s semiconductors use both features to decipher what is going on in our world.

Electron - a fundamental subatomic particle which carries a negative electric charge.It has a mass of 9.1 X 10-31 Kg, and an electric charge of 1.602 X 10-19 Coulombs (denoted as -e)The electron gives rise to the electromagnetic properties of the atom as well as the innate ability to chemically bond with the nuclei of adjacent atoms in nature. It can be bound to the atom or it can lead an independent life outside of the atom.
Electrons differ in the spin characteristics. These are denoted by quantum spin numbers.There are four quantum numbers which can describe the electron completely.
Principal quantum number(n)
Azimuthal quantum number(â„“)
Magnetic quantum number(m)
Spin quantum number(s): An electron has spin s = ½, consequently ms will be ±½, corresponding with “spin” and “opposite spin.” Each electron in any individual orbital must have different spins because of the Pauli exclusion principle, therefore an orbital never contains more than two electrons. Electrons that are free in a lattice or crystal for semiconduction retain their spin and the are always coupled to the other electron they are paired with no matter how close or far apart they are. This is called entanglement. No matter where that electron goes, the other electron contains informational and energy characteristics of the one another. If something happens to one, it must happen to the other electron, no matter where that electron is in the body or the universe.
Energy Levels - Electrons can only contain distinct quanta of energy. This is often represented graphically as having distinct energy levels or electron orbits.


GUT STRUCTURE LINKING TO ELECTRONS AND PROTONS: The FIAF is made by our liver, muscles, and our small bowel wall and when food sources (think electrons and protons) are in short supply. This means we must sense a paucity of electrons and protons across the entire system to create FIAF and subcutaneous fat that is common to our species. We know human evolution occurred in the East African rift zone and food from the ocean was plentiful.

Unknown said...

Peter you are well acquainted with FIAF already. FIAF builds the sub cutaneous fat mass in humans. FIAF grows when their is a scarcity signal. This implies that the gut microbiota has to take a lot of the electrons in food for themselves. This is also why the human gut shortened. When it shortened it helped craft the FIAF signal to develop sub cutaneous fat mass to support post natal brain growth. The second ecologic effect of a shorted gut is it created an island of isolation for the microbiota. This gave the human gut microbiome a severe diversity compared to other primates. Our teeth are very different from other primates as well and do not allow us to chew as well. This delivers more unprocessed food to this diverse microbiome which makes things for us that drive organ health in many places. The underpinning here is when you are isolating and shortening your gut for the microbiome it implies you can only do this when food sources with a dense source of electrons are present. this is the marine food chain. This is why human evolution began in the East African rift adjacent to the ocean. The electron is massless and can carry huge amounts of energy and information at a low thermodynamic cost compared to a proton. This is why humans have built their most complex systems, the brain and immune systems, around electrons and not protons. Protons are used to signal in the mitochondria the signals the environment provides. These signals then tell the cytochromes how to process foods.......in cytochrome 1 or two. The other cytochromes are used to signal the change programs in mitochondria, namely autophagy and apoptosis by opening a pore in the mitochondrial membrane to increase mitochondrial size. This is how heteroplasmy occurs. The better the redox potential the more heteroplasmy we see because it tells us the organism is best able to handle the changing signals in the environment. When the redox potential is not as good we employ too much apoptosis and not enough autophagy.......and we deplete stem cells. Where do the human stem cells come from? The most plastic human stem cell is in subcutaneous fat. To access those stem cells requires a massive stream of electrons in the sympathetic nervous system. Beta 3 agonists increase adiponectin and allow us to tap the stem cells.......alpha 2 agonists in SNS shut it off. Leptin resistance increases the alpha two pathway and shuts down the beta 3. And Peter, remember CD36 in the mouth we spoke about long ago? It stimulates the beta 3 agonist pathways. What else does? Cold weather. This is the pathway where ox/phos is uncoupled and the potential energy locked within the mass filled particle, the proton is used to alter the function of UCP1 to generate free heat and not make any ATP.

Unknown said...

And IFing also provides the scarcity signal needed to make a diverse microbiome........but it requires a good redox potential in the gut with exclusion of O2 within the lumen........to reserve electrons for us and give protons to the microbiome.

Unknown said...

Every wonder why human infants are born with no teeth and then develop a primary dentition that is more herbivore like.........and yet all human kids hate veggies and love meat and fish? FIAF. That is why. They need it to complete brain construction. The gut microbiome takes out the protons when O2 is lacking in the gut and reserves the electrons for brain construction. electrons are massless sources of energy and information........the perfect subatomic particle to build a brain with. Protons are a gut mitochondrial signaling molecule to allow things to talk to one another.

Puddleg said...

Great comment thread, sorry I missed it!
Jack, where I think the quantum potential of membranes/water might be used is in streaming ROS and other signalling molecules, and in streaming intermediate metabolites between enzymes. I don't believe these things just happen by random diffusion.

Puddleg said...

Here's a nice new paper about how HCV manipulates mitochondrial replication and autophagy to suppress mitochondrial interferon-activating signals (from MAVS) and harvest the autophaged mitochondrial goodies for its own replication.

http://www.pnas.org/content/early/2014/04/10/1321114111

Discussion here:
http://medicalxpress.com/news/2014-04-bad-mitochondria-mechanism-persistence-hepatitis.html

In response to viral infection, RIG-I–like RNA helicases bind to viral RNA and activate the mitochondrial protein MAVS, MAVS forms functional prion-like aggregates to activate and propagate, via the transcription factors IRF3 and NF-κB, type-I interferons (intracellular antiviral innate immune response).

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3179916/

Unknown said...

George water chemistry itself is quantum. Read Pollack's chapter on diffusion in his new book. The experiments are all done. No one seems to know it and even fewer are seeing how this directly ties to mitochondrial handling of electrons and protons.

Puddleg said...

Jack, as I see it the question is whether resonance structures and covalent-type quantum energy from a cell's structural lipids and proteins can create currents in the surrounding water, highways or conveyer belts for small molecules, that are also part of the structural organisation of the cell.

Puddleg said...

Linus Pauling on quantum mechanics of chemistry, 1960: http://tinyurl.com/mx8tvjl

Unknown said...

George here is my answer: http://jackkruse.com/hashimotos-and-melasma/The funny thing is mitochondria also live and die based upon their masses. The change programs in them are called autophagy and apoptosis. What controls mitochondrial swelling? The loss of massless energy, namely the electron. Mitochondria use electron loss to signal things to a cell over its collagen cytoarchitecture. A one-electron reduction of oxygen forms superoxide (02-), a two-electron reduction forms hydrogen peroxide (H2O2), and a three-electron reduction forms the hydroxyl radical (.OH). A rise in hydroxyl free radicals is called a Fenton reaction. Many other ROS species can be derived from superoxide and hydrogen peroxide. Generally the worse the environmental insult the more hydroxyl free radicals one gets. When this occurs, the mitochondria swell badly. It turns out, non native EMF cause these Fenton reactions to occur in mitochondrial rapidly and to a great degree. This causes electron steal syndrome in the mitochondria and this swelling signal is amplified all over a cell. When a mitochondria swells it is surrounded by water. This disturbs the water hydration cell around mitochondria by creating a larger proton layer in it, with respect to electrons. This altered balance of subatomic particles, alters the redox potential inside the cell. H2O, the atomic structure of water absorbs heat in the form of infra red radiation better than any source of electromagnetic part of the spectrum. Protons are positively charged and this drives inflammation. Water loaded with protons and devoid of electrons has a higher temperature in it. Why? As Gerald Pollack experimentally proved, hot water has a higher mass than cooler water does. Protons have mass, and electrons do not. Hot water has more protons in it. Cold water has more electrons in it. This is why cold water has more oxygen in it as well. Electrons are thermodynamically favorable to all complex life. Prior to the liberation of oxygen in our atmosphere, all life used protons to live. Electrons were not plentiful in the environment, therefore life did not use it. It also explains why, for 2.5 billion years life on Earth remained simple and not complex. This is why Archea and prokaryotes were the first types of life on this planet. Their waste product was oxygen. Eukaryotes evolved to use the oxygen they created. They absorbed a prokaryote, and turned it into a mitochondria. This emergent new form of life is called a Eukaryote. It formed by endosymbiosis. Me and Peter are on a crash course. I am just speeding the party up a bit.

Puddleg said...

Auckland University of Technology's critique of low fat high carb dietary guidelines.
Lay summary, detailed discussion, appendices and references.
Getting epidemiological about the case for LCHF as a public health measure, plus, the SFA defense lawyers sum up.
Something for everyone here.

https://scienceofhumanpotential.files.wordpress.com/2014/04/moh-dietary-guidelines-feedback-april-2014-revised-23-4-14.pdf

gunther gatherer said...

Another high fat guru passes away:

http://blog.sethroberts.net/

Bleeding or a clot caused it. Don't play games with your heart guys.

gallier2 said...

One could also say, stop doing so much sports, gunther. He keeled over during intensive effort like many others sports addicts before him.

James said...

I think it's a bit of a misrepresentation to call Seth Roberts a high fat guru.

Unknown said...

I told Seth at AHS 2011 where he would would kill him sooner than anything he believed. Sorry to say I was right. California steals electrons from mitochondria like made. Electron steal = poor autophagy = means poor ubiquination = heart failure irrespective of your diet.

Unknown said...

Autopsy by blog post?

We don't know why Seth died, and the possibilities are many, such as an undiagnosed abnormality like Marfan's. Until a real autopsy is done, it is absurd and crude to do so on these blogs trying to prove pet theories.

An open-minded intelligence like Seth's is rare, and he will be greatly missed.

Puddleg said...

True that.
If I keel over prematurely, will that be from genetics, from too much fat, from decades of too much sugar before that, from decades of drug abuse, from workplace exposures to toxins, from past exposures to radioactivity, from too much, or not enough exercise, from EMF, from deficiency of some unknown nutrient?
We'll never know. Even if my autopsy is posted on my blog (which I'd like: screenshot this if you'd like it too) we'll never know.
This business of hypothesising and experimenting is about good living, which it does affect with results we can be sure of, rather than dying, which comes to us by a thousand causes, and which we will hopefully never know about.
RIP Seth.

Christopher said...

Why are people still taking Jack seriously and giving him a forum? He has been thoroughly discredited by everyone from Carbsane to Nikoley to McEwen...

Anonymous said...

Hi Jack, I highly respect your relentless out of the box thinking, but this doesn't really jive with the observations:

More than ever

California, being the most populous state, has more people age 100 or older than any other state - 5,921 - although two dozen other states have more per capita, the census shows.

http://www.sfgate.com/health/article/Number-of-centenarians-grows-in-U-S-4264852.php

Cheers!

Melchior.

Unknown said...

Melchior.....why? Because most of their centenarians have these common ties......abundant raw seafood, a cold Pacific Ocean, and they live on many of the largest faults in the world. Those older folks also lived in a time where their environment was not overrun with today's technology. California's younger population is pushing it to bankruptcy because of how much sicker they have gotten in 30 years? Why? Silicon Valley. Most centenarians wont be there in the next 50 yrs. See to get old you have to have been healthy when young.......that is the story of why I told Seth what I did when in California. He even remarked to me he had never considered that. Sadly he left us too soon. He was a nice guy and a smart cat. I just left a slew of comment over at Bill's blog tied to this Melchior. You should look at them.

cwaiand said...

gulf war is caused by anti biotics.

quinolones .they were given cipro which destroyed their bodies(mine too).

cj

cwaiand said...

gulf war syndrome is caused by the overdose of anti biotics they were given.

quinolones.they were given cipro which destroys mitochondria(mine too).

cj

Unknown said...

And quinolones have what in them ? Fluoiride which is a dielectric blocker in water. It also inactivates electrostatic bonding of water to collagen leading to tendon tears and poor neurologic function because it displaces iodine in synapses that protect the double allylic PUFA bonds of DHA from oxidation.

The Role of Charge

Since a nucleophile is a species that is donating a pair of electrons, it’s reasonable to expect that its ability to donate electrons will increase as it becomes more electron rich, and decrease as it becomes more electron poor. So as electron density increases, so does nucleophilicity. There are 4 factors that affect nucleophilicity.
1. charge:
electron density increases charge. My bet is you have lost more DHA than you added via oxidation
2. electron negativity: Loss iodine and gain in fluoride or bromide means you can not use the electrons you do have because they tightly held
3. solvents: Likely tied to dehydration. Check your BUN/creat ratios.
A polar protic solvent like water can participate in hydrogen bonding with a nucleophile, creating a “shell” of solvent molecules around it like mobs of screaming teenage fans swarming the Beatles in 1962. In so doing, the nucleophile is considerably less reactive; everywhere it goes, its lone pairs of electrons are interacting with the electron-poor hydrogen atoms of the solvent.

The ability of nucleophiles to participate in hydrogen bonding decreases as we go down the periodic table. Hence fluoride is the strongest hydrogen bond acceptor, and iodide is the weakest and why it is used to protect DHA double bonds. This means that the lone pairs of iodide ion will be considerably more “free” than those of fluoride, resulting in higher rates (and greater nucleophilicity).

4.steric hinderance: Not likely a layer in your issue with a quinolone.
the bulkier a given nucleophile is, the slower the rate of its reactions because it has a higher atomic mass......

Higher mass means less energy.................due to mass equivalence

donny said...

Why is Christopher still worried about who people want or don't want to talk to? Why does he think it's somehow the world's duty to ostracize Jack Kruse?