Dr. Philip Lee Miller
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Dr. Philip Lee Miller

news and views for your optimal health and wellness

Anticoagulant Natural Alternative

Anticoagulant Natural Alternative

August 3, 2016 Philip Miller Comments 16 comments

Novel anticoagulant regimen to prevent strokes and heart attacks

Natural Anticoagulant Regimen

A natural anticoagulant routine. How could this benefit you? How can you implement this? Why is this a time-proven alternative to conventional approaches?

Hopefully, you have read part1, part2, and part 3 of this 4 part series. Primers on coagulation and thrombosis. I have carefully explained the process of coagulation resulting in heart attacks and strokes. We have talked about platelet aggregation. Which then leads to fibrin aggregation. Which leads to the final clot. All clots cause obstruction. Obstruction causes heart attacks and strokes. How can we prevent this?

I have alluded to the most powerful natural anticoagulants. These include the following:

  • Nattokinase — 100 mg twice daily
  • Ginkgo biloba — 120mg daily
  • High-dose fish oils — 1 tablespoon (10 grams) daily
  • Vitamin E — 800-1200 units daily
  • Adequate hydration — many glasses of pure water daily

Nattokinase

Nattokinase is a fibrinolytic anticoagulant. NSK-SD brandLet’s start with Nattokinase. Nattokinase is a derivative of the natto bean.  This is a Japanese food source. Nattokinase is a serine protease produced by Bacillus subtilisduring during fermentation. Nattokinase is very bitter to the taste!  Unpalatable. Therefore, the standardized extract is preferable and convenient.

Nattokinase is a fibrinolytic agent. You can refer back to all previous fibrin pathways. The goal is to prevent fibrinogen converting to fibrin.

Nattokinase has been studied extensively by the Japanese.  Nattokinase biochemical activity is labeled in FU. That is fibrinolytic units. These activity units have a mg equivalent. A typical dose is 100 mg (2000 FU) twice daily. It is essential that you take this twice daily. Once daily is insufficient.  This has been time proven through empirical observation.

I have treated thousands of cases with Nattokinase preventing recurrent thrombophlebitis, strokes and heart attacks.  It is essential that you source NSK-SD.

There are alternatives to Nattokinase.  Lumbrokinase is derived from the earthworm.  It is commonly sold as Bolouke in Canada.  By the manufacturer’s claims, it is even more potent.  Higher biological activity. Serrapetase has similar but not identical properties.  I use Serrapetase to treat arterial plaques.

Here is a great reference paper on the fibrinolytic and anticoagulant properties of Nattokinase.

 Ginkgo Biloba

ginkgo biloba is one of the most ancient plants on earth. anti-platelet anticoagulantGinkgo biloba has many actions. This is a time-honored and venerated Chinese herb. Ginkgo biloba has multiple constituents. These are flavonol and flavone glycosides, lactone derivatives (ginkgolides), bilobalide, and much more. We use a standardized 26% ginkgo extract. The Germans have studied this in detail.  Reference the German E Commission. Here is a more readable guide.

The dose I recommend is 120 mg daily.  Or 60 mg split twice daily. German studies have advocated as high as 240 mg. Through empirical observation, I find this dose to be way too aggressive. Ginkgo is so potent that 240 mg will probably cause adverse bleeding.

Ginkgo Biloba exerts its action primarily as an anti-platelet anticoagulant drug. It inhibits platelet aggregating factor. Ginkgo has many other uses. It is an antioxidant. Ginkgo may have vasodilatory effects. It is used for cognitive enhancement. I find it much more effective as a cardiac protective drug.

Be careful with your dosing ginkgo biloba. I advocate the use of 4Sight. This is a potent combination used to prevent eyesight deterioration. It includes 60 mg of ginkgo biloba. It is one example of adjusting the total dose of ginkgo biloba. And that is, again, 120 mg.

Because of its action, ginkgo biloba should not be combined with aspirin or NSAIDs. It will have synergistic effect.

High-dose fish oils

Fish Oil ProOmega rich in EPA and DHAHigh-dose fish oils have a “rheological” effect. That is the prevent aggregation of red blood cells. It is the aggregation of platelets and/or red blood cells is the initiating process. High-dose fish oils act like Teflon to prevent this aggregating effect. The dose that I recommend is aggressive. 1 tablespoon daily. You will rarely achieve these doses with oral capsules. I highly recommend fish oils in liquid form.

Fish oils contain EPA (eicosapentanoic acid) and DHA (docsoahexanoic acid).    I recommend 4000-5000 mg of EPA and 3000-4000 mg of DHA. That would total approximately 10 grams of fish oil. 1 tablespoon of high potency fish oil will yield this high dose of 5000 mg EPA and 4000 mg of DHA. I stress again, you will not achieve these doses with fish oil capsules.

Fish oils, in addition to their anticoagulant effect, may have multiple benefits:

  • enhance brain function – cognitive enhancement
  • prevent cardiovascular events
  • antidepressant
  • improve skin turgor
  • lower blood pressure
  • treat gastric reflux

Vitamin E

vitamin E tocopherolsVitamin E also has rheological properties.  It prevents red blood cell aggregation.  Vitamin E exists as a family of tocopherols.

I highly recommend mixed tocopherols. This is a isomeric mix of natural tocopherols including the alpha, beta, gamma and delta forms of vitamin E. There is a difference between “natural” vitamin E and “synthetic” natural vitamin E. Synthetic vitamin E is a tocopheryl not tocopherol.

I routinely recommend a 400-800 units of mixed tocopherols (vitamin E) daily. In many instances I will recommend 800-1200 units of vitamin E.  Studies have shown that Gamma tocopherol is much more potent than alpha tocopherol. Most studies only investigate the alpha form of Vitamin E.

Water – Hydration

bottled water in glass is free of plasticizers And last but not least, hydration. Keep well hydrated. Hydration will also prevent red blood cell and platelet aggregation. It will improve skin turgor.  I highly recommend water in glass bottles, not plastic bottles. You should avoid all plasticizers.  PVCs, phthalates and BPA. The softer the plastic bottle the higher the plasticizer content.  Never tap drink water.  Most likely, all your municipal water sources are contaminated or polluted.  Chlorine, chloramine, flouride, and heavy metals. Flint Michigan is just the tip of the iceberg.

Potency and efficacy

So this routine when fully implemented will prevent platelet and red blood cell aggregation. It prevents the conversion of fibrinogen to fibrin. This treats all pathways of coagulation. It is a much more comprehensive approach to anticoagulant therapy than conventional drugs. Less expensive. With fewer complications. Is it effective?

Virtually every surgeon now has been taught to ask, “what other vitamins and herbs are you taking?” Every surgeon knows that each and all of these agents clearly have anticoagulant effects. Surgeons see the effects of drugs. Internists only infer the effects of drugs. Surgeons know that prior to surgery anticoagulants can significantly increase complications. However, just following surgery the opposite effect is noted. The body may react with a vigorous coagulation response.

So empirically and rationally you can see this routine has the ability to effectively prevent heart attacks, strokes and recurrent thrombophlebitis.

Medical Supervision is Essential

Physician Supervision is within your reachA major caveat! I never advocate abruptly stopping conventional anticoagulant routines. You need medical supervision to start and monitor your progress. This anticoagulant routine requires special knowledge of potency, dosing and the value of these natural sources. I have been treating thousands of cases over the past 20 years. This is time-tested. It is effective. But this regimen is not “validated” through conventional guidelines or task force committees. It is not the “standard of care.” For this reason, your internist, cardiologist or family practitioner will have little understanding of the rationale or efficacy of this routine.

This is not a DIY — do it yourself advocacy.

So where do we go from here? Let me give you some suggestions.  Call us or write for further information.

[email protected]

call 408-358-8855

AntiPlatelet AntiCoagulant Drugs

AntiPlatelet AntiCoagulant Drugs

August 1, 2016 Philip Miller Comments 2 comments

Coagulation and Anticoagulatant Therapy

Read part I and part II of this series for background.  So you will have a basic understanding of coagulation pathways. Yes, it is complex.

Remember, coagulation or clotting starts with platelet aggregation.  That initiates the complex coagulation cascade. This causes the mature thrombus or blood clot. Aggregated platelets with a thick fibrin mesh causes the thrombus.  The thrombus causes heart attacks, strokes or thrombophlebitis.  Here is the final complete picture:

injury activates platelets causing thrombus formation
fig 1- click for full size

So let’s discuss anticoagulant therapy medications.

Antiplatelet Agents – Aspirin and Plavix are first line of defense

Figure 2 shows how we prevent platelet aggregation and activation at various stages.  Look at figure 1.  Aspirin has been the mainstay of antiplatelet therapy. There has been a succession of drugs over the last three decades. Newer antiplatelet drugs supersede older ones.  Are these true advances or simply marketing campaigns?

antiplatelet drugs classified by site of action. Aspirin and Plavix are the most common platelet inhibitors
fig 2 – click for full size

Aspirin has been well studied in the literature.  A full 325 mg dose will prevent platelet aggregation.  Over time, aspirin has significant adverse reactions. These are direct and indirect reactions. It can cause tinnitus (ringing or buzzing noises in the ear).   It can cause major gastrointestinal bleeding.   This is a significant problem.

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Coagulation Heart Attack and Stroke – Part 2

Coagulation Heart Attack and Stroke – Part 2

July 18, 2016 Philip Miller Comments 0 Comment

It is necessary to understand the interaction of fibrin coagulation pathways and platelet aggregation. Once we understand these interactions we can then discuss current treatment modalities. My goal is to show you a more creative and natural approach to anti-coagulation.

Initial Platelet Aggregation

activated platelet aggregation
fig 1

In part one I emphasized the importance of platelet aggregation as the initial step.  There is an initial injury to an arterial or venous wall.  As a response, activated platelets cause a clumping reaction to repair the injury.  Somewhat like Hans Brinker’s “finger in the dike.”

This injury could be a laceration. It could be a rupture of a atheromatous plaque. It could simply be a tear in an arterial wall.   Or simply from low-flow stasis.  Atrial fibrillation is an example.

 

platelet activating factor PAF
fig 2

You can see from fig 2 above that the platelets initiate an array of reactions.  I will elaborate even more detail in the next post.  This is ever-increasing overview.

Aspirin is the most common drug to prevent platelet aggregation.  We will look at an array of  drugs that have been used over the years. But there is a more creative approach.

Once the initial platelet plug has formed the long-term fibrin coagulation pathway is initiated. 

 Fibrinogen pathways

fibrin to fibrinogen cascade from intrinsic and extrinsic pathways
fig 3

The classic fibrin clotting pathway is divided into the intrinsic and extrinsic systems. The intrinsic system starts with Factor XII.  There is a cascading series of reactions to the final common pathway. This is prothrombin activating thrombin. Thrombin then catalyzes the reaction of fibrinogen to fibrin. Finally, fibrin is polymerized to an insoluble mesh.  The extrinsic arm interacts with the intrinsic arm.

As discussed previously, the production of fibrin can be blocked at various stages.  The conversion of fibrinogen to fibrin can be reversed through a process called fibrinolysis.  An important concept.

So now we have a complete picture. The following diagram summarizes the evolution of this thrombus from platelet aggregation to fibrin clot.

Decision-making – Blocking Which Pathway?

Now we have rapidly covered the two aspects of thrombosis (clot) production.    This is where the subject becomes indeterminate.  Some “guidelines” emphasize the prevention of platelet aggregation. While other guidelines emphasize the long-term use of anti-fibrin drugs.  What is the best strategy? Depends on the guidelines.  These evolving guidelines are determined by age, associated risk factors, and preceding condition.

These guidelines were originally developed to make decision-making simple. And uniform. And coherent. The community standard of care. But guidelines eventually become bloated and incoherent. Much like IRS tax code. I anticipate this decision-making process will soon be totally computerized.  Remove the human discretionary input. I do not agree.   Look here to see just how complex this decision tree for anticoagulant therapies can be.

The entire purpose of this series of posts is to present a novel combination of anti-fibrin anti-platelet modalities.

Now you have an overview of the basic flow.   In part 3 we will examine current and past drug interventions.

Coagulation Stroke Heart Attack Part 1

Coagulation Stroke Heart Attack Part 1

July 15, 2016 Philip Miller Comments 0 Comment

Heart Attack and Stroke Coagulation Basics

Let’s talk about heart attack and stroke causes and the complexity of the underlying coagulation (clotting) pathways.    What a heady subject.    You need a PhD in medical hematology, just to fully understand the complexities of coagulation.   So let’s work through this step by step.  This will be a multi part series.  I will help you achieve a clearer understanding. None of us wants to suffer a heart attack or stroke!

What causes these these catastrophic vascular events? What are the risks?  What medications are commonly used?    Why are they not necessarily the best or even the healthiest choice?   Can we assess risk benefit ratios?   And what are the natural herbal-based alternatives?  Ones that can be just as effective with fewer side effects and less costly.   This is what you will not hear from your personal internist, cardiologist or even family physician.

Blood Clot is a Thrombus or Embolus

A thrombus totally blocks (occludes) blood flow from activated coagulation factors
fig 1

A blood clot usually starts with an injury to a vascular wall.  This could be one of your arteries or veins.  An intricate series of reparative or reactive events is set in motion.   Your body tries to rapidly repair injury to the vascular wall.   Atrial fibrillation is an alternative source of thrombus formation.  In this instance, stasis and not injury, initiates the reaction.

Fig 1  above shows you a representation of the well formed blood clot. It has the potential for blocking blood flow (vascular occlusion) which deprives tissues distal to the block of vital cell oxygenation. The medical term is myocardial infarction or cerebral infarction. Cells die from lack of oxygen.

The initial early phase begins with activation and aggregation of platelets.

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Hashimoto’s Thyroiditis and Reverse T3 Thyroid

Hashimoto’s Thyroiditis and Reverse T3 Thyroid

June 5, 2016 Philip Miller Comments 16 comments

 

Hashimoto's can affect normal T3 and T4 physiology]

Hashimoto’s Auto Immune Thyroiditis

Hashimoto’s is an auto-immune condition.  Where your body sees thyroid as “foreign” or “not self.”  This stimulates production of antibodies against to your own thyroid.  There are a host of auto immune conditions including Sjogren’s (Sicca Syndrome). Lupus, Scleroderma, CREST Syndrome and Rheumatoid Arthritis.

[Important note: It is vital to recognize that the TSH test is being used as a screening test.  See previous blog.  It will not diagnose Hashimoto’s.  It will totally miss this condition for years.]

We measure two antibodies.  Anti-thyroglobulin (matrix of the thyroid gland) and TPO (thyroid peroxidase).   TPO is essential to the conversion of T4 to T3.   Either of these can rise with Hashimoto’s.   It is more common to see a rise in the TPO.    This condition usually results in Hypothyroidism (under active thyroid) by interfering with the normal conversions.   The normal flow is T4 converts to the active form T3.  The more technical term is Hashimoto’s Autoimmune Thyroiditis.  It can occasionally result in the opposite.  That is, hyperthyroidism (over active thyroid) during a more acute or sub acute inflammatory phase.   Thyroiditis means inflammation of the thyroid.

What causes Hashimoto’s?  This is not really well known.  There are various theories.  You will read that there are genetic factors.  And, it is far more common in women than men.  It is quite unusual in men.

 

Speculative (unproven) theories

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Tyranny of the TSH

Tyranny of the TSH

May 23, 2016 Philip Miller Comments 2 comments

The Tyranny of the TSH

Let’s talk about further thyroid testing.  In an effort to reduce laboratory costs and find ever cheaper methods of evaluating thyroid function, the TSH has become the more commonly accepted first line test with “reflex” follow-up.

Now this assumes three very important concepts.

  1. The feedback mechanism between the pituitary and the thyroid is intact and functional.
  2. It assumes a “normal distribution.” That is, a typical “bell shaped” curve of all values from low to high.
  3. That we can assign “reasonable” upper and lower cut-off values.

Idealized Thyroid Feedback

Refer to figure 1.  You can see that TSH is part of a functional feedback loop.   High values infer hypothyroidism (under-active thyroid) and low values infer hyperthyroidism (over active thyroid).   The TSH values are opposite (inverse) to thyroid activity.  A compensatory mechanism.

thyroid schema
fig 1

But there is human variation.  It is an idealized loop that is not as precise as an integrated circuit.  A result of overly simplified mechanistic thinking.  There are rare situations where hypothalamic dysfunction can cause very low TSH levels rather than feedback from low thyroid activity.  This is termed central hypothyroidism.

We have steadfastly maintained over the last 15 years that complete thyroid analysis should include a TSH, free T4 and a free T3.  Frequently adding the reverse T3 and thyroid antibodies.  Refer to our previous post.   The TSH is a poor measure of free T3 — the active metabolite or driver of metabolic function.

What is a Normal Distribution?

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Aging Research Topics and Meetings

Aging Research Topics and Meetings

May 20, 2016 Philip Miller Comments 0 Comment

Aging and Age-Related Conferences and Updates:

Fotolia-meeting2

[We are indebted to John Furber for these timely and comprehensive updates on aging and anti-aging research, meetings and conferences]

(updated 9 April 2016)

 

Disease Drivers of Aging: 

2016 Advances in  Geroscience Summit

April 13-14, 2016, New York City

Co-sponsored by AFAR, GSA, NIH, NYAS

www.nyas.org/Geroscience2016

 

Cognitive Aging Conference

April 14-17, 2016, Atlanta, Georgia, USA

http://cac.gatech.edu/

 

31st International Conference

Alzheimer’s Disease International

April 21-24, 2016, Budapest, Hungary

http://www.adi2016.org/

 

Biomedical Innovation for Healthy Longevity

April 25-28, 2016, St. Petersburg, Russia

http://www.ivaoconf.org/

 

There’s much more … …

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The Why and How of Thyroid Dosing

The Why and How of Thyroid Dosing

April 10, 2016 Philip Miller Comments 4 comments

Thyroid assessment and treatment

Your thyroid is a master controller of vital human functions.  It controls your rate of metabolism and is the seat of your immunity.     There is an array of firmly held opinions, explanations and approach to treatment.

Characterization and symptoms

Hypothyroidism, an under active thyroid gland,  is common and is a frequently under-treated or un-treated endocrine disorder.     It is characterized by any of a number of symptoms including:

  • fatigue
  • weight gain or inability to lose weight
  • depression
  • poor immunity
  • cold hands or feet
  • hair loss
  • dry skin
  • low body temperatures
  • constipation
  • cognitive impairment (foggy brain)
  • puffy eyelids or loss of lateral eyebrows

Thyroid Cascade and Control

The approach to thyroid disorders is steeped in tradition, dogma and lack of understating of basic physiology and biochemistry.

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aging conferences update

aging conferences update

February 25, 2016 Philip Miller Comments 0 Comment

Aging Related Conferences

[with special thanks to John Furber]

Aging Conference schedule
A Look at the future of aging

 

Aging research meetings calendar (updated 5 April 2018)

______________________
John D. Furber
Legendary Pharmaceuticals
PO Box 14200
Gainesville FL 32604-2200
email:    [email protected]
http://LegendaryPharma.com/chartbg.html
______________________
 compiled by John Furber
La Jolla Aging Meeting (LJAM)
April 13, 2018, Salk Institute, La Jolla, California
9 am – 5 pm
Registration required, but Attendance is FREE.
Registration deadline: March 30, 2018
Posters welcome. Lunch and reception included.
https://www.salk.edu/events/science-events/la-jolla-aging-meeting/
Age and Longevity in the 21st Century: Science, Policy and Ethics
Global Bioethics Initiative and New York Medical College
April 13-15, 2018, Manhattan, New York
THEMES:  Aging research, Regenerative medicine, Cryonics, Healthy life extension.
www.conferenceaging.org
Keystone Symposium 
“Pushing the limits of Healthspan and Longevity”
April 15-19, 2018, Herrenhausen Palace, Hannover Germany.
Scientific Organizers:  Rochelle Buffenstein, Holly Brown-Borg, Colin Selman.
http://keystonesymposia.org/index.cfm?e=web.Meeting.Program&meetingid=1529
[ !! If you go to Hannover, maybe take a train from Hannover to Kazan, Russia !!]
EB2018 Experimental Biology
April 21-25, 2018, San Diego, California
Abstract submission deadline is December 7, 2017
Early Registration Deadline: February 27, 2018
Hotel Reservations Deadline: March 28, 2018
http://experimentalbiology.org/2018/Program/Preliminary-Program.aspx
Interventions to Extend Healthspan and Lifespan
April 22-26, 2018, Kazan, Russia
4 days; 40+ speakers.
Registration fee is about US$ 87.
It is impossible to obtain an entry visa upon arrival, so travelers must apply for their visas well in advance.
   http://www.russianembassy.org/page/important-visa-information
You can reach Kazan by rail or by air from Moscow or St. Petersburg.
   https://waytorussia.net/Kazan/Transport.html
Kazan is on the Trans-Siberian Railway, on the ancient Silk Road, for those wanting to travel by rail via Beijing or Vladivostok or Moscow.
   http://www.trans-siberian-travel.com/trans-siberian-journeys/route-map.html
   http://extendlifespan2018.org/
3rd ISANH Middle East World Congress
Amman Antioxidants World Congress 2018
Royal Scientific Society of Amman, Jordan,
under the patronage of HRH Princess Sumaya bint El Hassan
The Scientific Committee invites all scientists, academics, and industrials to present their researches in antioxidants and nutraceutical and functional ingredients.
May 2-3, 2018, Amman, Jordan
Chair: Professor Richard G. Maroun
Early registration discount by Feb 21.
www.isanh-me.com
Mitochondrial Medicine
May 9 – 11, 2018, Wellcome Genome Campus, Hinxton, Cambridge, UK
https://coursesandconferences.wellcomegenomecampus.org/events/item.aspx?e=701
Bay Area Aging Meeting
May 17, 2018, University of California, Berkeley
Li Ka Shing Center, Room 245
Please register for FREE at http://agingmeeting.org/registration/
Food provided.
The purpose of the semiannual Bay Area Aging Meeting (BAAM) is to stimulate the advancement of aging research, promote its application to human health and to connect scientists throughout the Bay Area to facilitate collaboration.
Multifaceted Mitochondria
Cell Symposia
June 4-6, 2018, San Diego, California
Abstract submission deadline: February 12, 2018
http://www.cell-symposia.com/mitochondria-2018/default.asp
http://www.cell-symposia.com/mitochondria-2018/conference-speakers.asp
SFRRI 2018, 19th biennial meeting 
June  4-7, 2018, Lisbon Portugal
http://sfrri2018lisbon.organideia.pt
Symposium on Aging and Anti-Aging
Center for Integrative Genomics (CIG)
2018 CIG Symposium
June 21-22, 2018, University of Lausanne, Switzerland
Organizer: Winship Herr
http://www.unil.ch/cigsymposium/home.html
Harvard/Paul F. Glenn Symposium on Aging
June 25, 2018, Harvard Medical School, Boston, Massachusetts
Monday, 1:00 – 5:00 pm.  Please register Free online at:
     http://www.hms.harvard.edu/agingresearch/index.php/events/symposium
Here, you can also download the upcoming program, as well as past programs and photos.
20th ISANH International Conference on Oxidative Stress Reduction, Redox Homeostasis & Antioxidants
Paris Redox 2018
International Society of Antioxidants in Nutrition and Health (ISANH)
June 25-26, 2018, The Université Pierre et Marie Curie, Paris, France
President: Prof. Frédéric Batteux, University Paris Descartes, France
www.isanh.net
American Aging Association 47th Annual Meeting
“Improving Resilience to Delay Aging”
Held in conjunction with the Nathan Shock Centers’ Summit. 
June 27-July 1, 2018, Philadelphia, Pennsylvania
Abstract deadline May 27.
http://www.americanagingassociation.org/meeting/program
http://www.americanagingassociation.org/
Fourteenth International Symposium on Neurobiology and Neuroendocrinology of Aging
July 15-20, 2018, Gasthof Hotel Lamm, Bregenz, Austria
Organizer: Holly M. Brown-Borg, Ph.D., Univ of North Dakota
www. Neurobiology-and-neuroendocrinology-of-aging.org
Matrix Biology Europe 2018
July 21-24, 2018, University of Manchester, Manchester, UK
Abstract submission for the oral presentation will close May 18, 2018.
Early bird rates for registration ends June 15.
http://www.confercare.manchester.ac.uk/events/mbe2018/
Alzheimer’s Association International Conference (AAIC)
July 20-26, 2018, Chicago, Illinois, USA
https://alz.org/aaic/
View AAIC 2017 conference abstracts here. No login is required.
Cold Spring Harbor Laboratory meeting on 
Mechanisms of Aging
October 1-5, 2018, New York
Abstract Deadline: July 13, 2018
Organizers:  Vera Gorbunova, Malene Hansen, Scott Pletcher
https://meetings.cshl.edu/meetings.aspx?meet=AGING&year=18
Jena Aging Meeting (JAM)
September 6-8, 2018, Jena, Germany
Leibniz Institute on Aging – Fritz Lipmann Institute (FLI)
Abstracts deadline is April 15, 2018.
Early registration discount until April 15, 2018.
http://www.leibniz-fli.de/jam2018
New Scientist Live
September 20-23, 2018, London
International Bordeaux Conference
“Aging of memory functions: Where are we now?”
September 26th-28th, 2018, Bordeaux.
Contact:  Nora Abrous <[email protected]>
12th World Congress on Polyphenols Applications
Bonn Polyphenols 2018
September 26th-28th, 2018, Bonn University, Germany
Early registration by March 7.
www.polyphenols-site.com
International Conference on Aging and Disease (ICAD)
International Society on Aging and Disease (ISOAD)
October 5-7, 2018, Nice, France
    You are encouraged to submit your abstract as early as possible.
Home page at  www.isoad.org
Speaker List is at   http://www.isoad.org/Data/List/Conference
AABB Annual Meeting
October 13-16, 2018, Boston, Massachusetts
The AABB Annual Meeting is the premiere event for healthcare professionals in the fields of transfusion medicine and cellular therapies.
http://www.aabb.org/
American Society for Matrix Biology (ASMB) Biennial Meeting
October 14 – 17, 2018, Las Vegas, Nevada
Early bird discount before July 8.
www.asmb.net
10th International Conference on Heme Oygenase 
November 1-3, 2018, Ulsan/Geongju, South Korea
Organized by Prof Hun Taeg Chung and Prof Young-Joon Surh.
Society for Neuroscience – Annual Meeting
November 3-7, 2018, San Diego, California
www.sfn.org
Fourth Eurosymposium on Healthy Ageing (EHA)
November 8-10, 2018, Brussels, Belgium
http://www.eha-heales.org/
Gerontological Society of America (GSA)
Annual Scientific Meeting
November 14-18, 2018, Boston, Massachusetts
Regular abstracts  closed March 15, 2018.
The late breaker poster submission will open in July and close September 13, 2018.
https://www.geron.org/meetings-events/future-gsa-annual-scientific-meetings
A4M 26th Annual World Congress
December 13 – 15, 2018, Las Vegas, Nevada
https://www.a4m.com/world-congress-2018/home.html
Gordon Research Conference on Aging, Biology of
“The Translational Science of Aging: From Functional Pathways to Interventions”
July 14-19, 2019, Sunday River, Newry, Maine, USA.
Application deadline is June 21, 2015
https://www.grc.org/biology-of-aging-conference/2019/
Chairs:  Marcia C. Haigis and Thomas Rando
     ( Note: An affiliated Gordon Research Seminar for graduate students and postdocs will take place on the preceding two days, July 13-14.  Separate registration is required. https://www.grc.org/biology-of-aging-grs-conference/2019/  )
Gerontological Society of America (GSA)
Annual Scientific Meeting
November 13-17, 2019, Austin, Texas
https://www.geron.org/meetings-events/future-gsa-annual-scientific-meetings
Gerontological Society of America (GSA)
Annual Scientific Meeting
November 4 – 8, 2020, Philadelphia, Pennsylvania
https://www.geron.org/meetings-events/future-gsa-annual-scientific-meetings
Gerontological Society of America (GSA)
Annual Scientific Meeting
November 10 – 14, 2021, Phoenix, Arizona
https://www.geron.org/meetings-events/future-gsa-annual-scientific-meetings
Gerontological Society of America (GSA)
Annual Scientific Meeting
November 2 – 6, 2022, Indianapolis, Indiana
https://www.geron.org/meetings-events/future-gsa-annual-scientific-meetings
Gerontological Society of America (GSA)
Annual Scientific Meeting
November 8 -12, 2023, Tampa, Florida
https://www.geron.org/meetings-events/future-gsa-annual-scientific-meetings
Gerontological Society of America (GSA)
Annual Scientific Meeting
November 13 – 17, 2024, Seattle, Washington
https://www.geron.org/meetings-events/future-gsa-annual-scientific-meetings
####### END OF AGING RESEARCH MEETINGS LIST #######
Compiled by John Furber.
Several other lists on related topics are at the following websites:
AgingPortfolio.org:  http://agingportfolio.org/events/
JenAge Information Centre:  http://info-centre.jenage.de/ageing/meetings-calendar.html
The Oxygen Club of California:  http://oxyclubcalifornia.org/OCC/upcoming_meetings.php
Society for Free Radical Research International: http://www.sfrr.org
FASEB Scientific Meetings: http://faseb.org/Home.aspx
FASEB Science Research Conferences: http://faseb.org/Science-Research-Conferences.aspx
Global Healthspan Policy Institute: https://healthspanpolicy.org/world-healthspan-calendar/
Gordon Research Conferences: http://www.grc.org
Keystone Symposia: http://www.keystonesymposia.org/
Alzheimer’s Research Forum:  http://www.alzforum.org/res/res/conf/default.asp
GSA List:  https://www.geron.org/meetings-events/events-calendar/cat.listevents/
UCL Consortium for Mitochondrial Research:  http://www.ucl.ac.uk/mitochondria/meetings
A variety of biology-related slides and posters are listed at F1000Research: 
http://f1000research.com/browse
======================
See some of the excellent interviews and lectures online at http://thesciencenetwork.org
For example:
     **  Stem Cells on the Mesa
     **  20 Jan 2011 Barzilai and Cuervo on The Science Network
http://thesciencenetwork.org/programs/new-york-city-january-2011/nir-barzilai-and-ana-maria-cuervo-1
======================
http://www.glennfoundation.org/media/
======================
Poster and oral presenters may wish to deposit their posters and slides in the Open Access F1000Research website, so that more people can see them.
       http://f1000research.com/
======================
You might also find the following of interest:
http://www.nejm.org/do/10.1056/NEJMdo005102/full/?query=TOC
QUICK TAKE VIDEO SUMMARY
Brain–Computer Interface in a Locked-In Patient
Patients with brainstem strokes or degenerative disorders such as ALS might have normal cognition without the ability to move or speak. A brain–computer interface enables autonomous communication, New research findings are summarized in a short video.
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Anti-Aging Medicine — the Promise of a better tomorrow

Anti-Aging Medicine — the Promise of a better tomorrow

January 29, 2016 Philip Miller Comments 0 Comment

Anti-Aging Age Management Medicine

the Future of Health and Wellness

looking for the right path and highway to the future
finding the road to the future

Anti-Aging Medicine / Age Management Medicine.  What is it?   Is it real? Are there real controversies here? In a word, yes.   Can it be fulfilled in today’s guideline, task force, economic environment?

We are poised at a very important juncture.   Anti-aging medicine offers promise of a goal oriented path to optimal health and well being.  Or we can pursue restrictive policy driven, algorithms of cookbook medicine.

What needs to change?  What gives it the stamp of approval?   Is it science or politics?  As the great philosopher Schopenhauer said:

“All truth passes through three stages. First it is ridiculed. Second, it is violently opposed. Third, it is accepted as being self-evident.”

There is a plethora of terms that have been spun off to better describe this new field. Longevity Medicine, Age Management Medicine, functional medicine, integrative medicine. These are all descriptions in pursuit of a new paradigm.

All medicine has from the beginning, most notably Hippocrates, been an effort to mitigate illness and suffering with the implicit goal of increasing life span. One yardstick could simply be life span or longevity. But we are more interested in quality of life. And here is the key. Increasing HealthSpan. It is about “squaring the curve” — living longer in a healthy, vibrant, vigorous, independent, and happy state of health and well being.

The paradigm shift is tectonic. We don’t have a health care system. We have a disease management system. All ICD-9 (now ICD-10) codes are a codification of disease. If you feel weak, fatigued or just “not right” you may not be suffering from a disease.   You can have a battery of tests and nothing will “show positive” for a disease.  You have a dysfunction. Pre-menopause is not really a disease. Yet it lasts for upwards of 4-5 years and can be seriously disabling. A dysfunction. Andropause is not even widely recognized as such. It is also a dysfunction that men suffer later than menopause. There is no formal ICD-10 code for andropause — just hypogonadism.

The wonderful medicine of the last 50 years has been disease-based , pathology-oriented with the goal of finding the right drug to cure or mitigate your disease. But there is a rapidly growing residua of conditions and patients who are not right, dysfunctional, that do not respond to the conventional or traditional approach. …

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