StemCell Therapy

Fat vs. Bone Marrow Stem Cells: A Clinicians Perspective

This week I treated a patient with adipose SVF stem cells to augment a low stem cell yield from bone marrow. I dont do this often, as the quality of fat stem cells for orthopedic applications like arthritis is much less. We do use fat for an occasional structural graft in various procedures. Today I wanted to give you a clinicians eye view of the harvest procedures for both stem cell types that you wont see elsewhere, so let Fat vs Bone Marrow Stem Cells begin.

In summary, harvesting fat in a mini-liposuction is a violent affair, harvesting stem cells from a bone marrow aspirate is like an advanced blood draw. Let me explain.

In order to get fat through a mini-liposuction you need to first use a scalpel to open a small incision in the skin. This isnt at all required for a bone marrow aspiration as the needle is just inserted into the skin like any other needle. In the liposuction, the whole goal is disrupting large amounts of normal tissue. In fact, the stem cells live around the blood vessels, so you have to chew up as many blood vessels in the fat as possible to get a good stem cell yield. This involves placing a small wand like device under the skin and into the fat and moving it back and forth (through much resistance) to break apart large sections of tissue. The bone marrow aspiration simply involves directing the needle under the x-ray to the desired area of bone. The needle is then turned back and forth a few times to enter the bone (which is like hard plastic instead of cement). At this point in the liposuction the doctor must continue to break up large swaths of tissue with suction, sucking the broken tissue and blood vessels into a syringe. On the other hand, in the bone marrow aspiration the doctor simply draws the bone marrow aspirate (which looks like blood) into the syringe like a common blood draw.

The complication rates for these two procedures tell the rest of the story. Mini-liposuction procedures have surgical style complication rates of 3-10%, while bone marrow aspiration complication rates are so rare that only a handful occurred in more than 20,000 procedures in one U.K. registry. The upshot? It always makes me chuckle (in a bad way) when I hear fat stem cell advocates claim that a bone marrow aspiration procedure is so invasive. Youhavent seen invasive until youve seen a lipo-suction!

Disclaimer: Like all medical procedures, Regenexx Procedures have a success & failure rate. Not all patients will experience the same results.

If you liked this post, you may really enjoy this book by the same author - Dr. Chris Centeno

Written by Regenexx Founder, Dr. Chris Centeno, this 150 page book explains the Regenexx approach to patients and orthopedic conditions. Whether youre are an existing patient or simply interested in the human body and how everything in the body ties together, you will enjoy exploring this book in-depth. With hyperlinks to more detailed information, related studies and commentary, this book condenses a huge amount of data and resources into an enjoyable and entertaining read.

Chris Centeno, M.D. is a specialist in regenerative medicine and the new field of Interventional Orthopedics. Centeno pioneered orthopedic stem cell procedures in 2005 and is responsible for a large amount of the published research on stem cell use for orthopedic applications. Centeno regularly lectures on regenerative medicine and has spoken twice at the Vatican Stem Cell Conference.

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Fat vs. Bone Marrow Stem Cells: A Clinicians Perspective

Our story began in the 1970s with a young student in a lonely laboratory. So consumed with his work, he barely had time to attend to classes. So advanced, that his education was not found in books, but in the fabric of what makes us human: our DNA. His dedication is now legendary, and his work set in motion countless genetic discoveries, including the Human Genome Project, the first initiative to map all genes in the human genome. Today, Dr. George Church is a recognized giant in genetic science and one of the co-founders of Veritas Genetics. Along with an esteemed group of visionaries and scientists, including a few from Harvard Medical Schools Personal Genome Project, Church and Veritas Genetics have become the leader in genetic sequencing and interpretation. It took 10 years and nearly $3 billion dollars to sequence the first whole human genome. Now, were delivering it into the palm of your hand in a matter of weeks, all for less than half the cost of the average family vacation.

Excerpt from:
Veritas Genetics - Committed to disease prevention, early ...

Ever since the cellular clock called telomerase was discovered, it was hailed as the next big thing in anti-aging research. And the science world has been divided in two. One side evoked unlimited cell regeneration that might make degenerative diseases a memory of the past. The other side cautioned us that cancer cells unlock telomerase to make themselves immortal while hastening our own death. So where lies the truth? This is exactly what youll find out in these 8 frequently asked questions on telomeres, telomerase and aging. Read on.

Q: What exactly is telomerase?

A: Lets start with what telomeres are: repeated units ending linear(eukaryotic) chromosomes. They are normally deleted with each cell division. Once the cell reaches the maximum number of divisions (also called the Hayflick limit), it remains in this state for some time and then dies.

Some cells do not like being limited and they add back their telomere units with the help of an enzyme called telomerase. This way, telomere length stays the same despite repeated cell divisions. Which brings us to the next question.

Q: Do all cells express telomerase?

A: No, they dont. When it comes to humans, telomerase is expressed in cells that are needed for development germ cells during replication and embryo cells or regeneration stem cells. Cancer cells use telomerase as well. All the other cells are inhibited from expressing it.

Before we move even further, lets stop for a moment and clear something up: not all cells normal or not use telomerase expression to keep on dividing. More to the point, some cells are able to add back telomeric units with the help of ALT or the alternative lengthening of telomeres.

Telomerase is not equally expressed during the life cycle of an organism, of its tissues or of its cells. Telomerase peaks in proliferative tissues and it is downregulated in postmitotic ones. Even in colonial animals like the Botryllus schlosseri golden star tunicate, telomerase peaks in bud rudiments and further decreases in its zooids. In other words, telomerase activity peaks in progenitor and stem cells and it is downregulated during differentiation. Telomerase is highly expressed in cells which actively divide and it is downregulated during quiescence.

Telomerase differences exist between growth patterns as well. Mammals grow only during the embryonic and juvenile stages. They exhibit determinate growth. On the other hand, species with indeterminate growth often express telomerase in their somatic cells. They grow throughout their lives and often exhibit very slow senescence.

And when it comes to plants, the latter have two types of tissues:

Q: But do all species inhibit telomerase in their adult somatic cells?

A: The short answer is no.

Poikilotherms or cold-blooded animals like invertebrates, fish, amphibians and reptiles persistently express telomerase in adult somatic tissues. This could have an impact on their regeneration abilities. Temperature increases metabolism, hence it may increase cancer mutation rates and endotherms do have higher metabolic rates than poikilotherms. This could be the reason for which endotherms or warm-blooded animals like birds and mammals supress telomerase in their adult somatic tissues as a cancer-protection mechanism.

Q: Which are the telomeric parameters that modulate long lifespans?

A:There are a set of important parameters to study in long-lived species:

Q: How does absolute telomere length influence lifespan?

A: Generally speaking, telomere length is indirectly proportional to lifespan. In other words, short telomeres are associated with long lifespans and viceversa.

Well start by examining the telomere length of humans, then rodents, sea urchins and turtles. The first two examples are gradual senescence species while the latter display negligible senescence signs.

The length of human telomeres is 10-15 kb.

Unlike humans, rodents have extremely long telomeres of 25-150 kb which dont decrease with age. Rodents have a much higher cancer rate than humans. Rodents usually have telomeres that are longer than 30kb and telomerase activity seems to inversely correlate with body mass. In other words, larger rodents express less telomerase. And when it comes to rodents, there is no correlation between telomere length with size or lifespan. But lets go further to negligible senescence species and how they fare about telomere length.

In sea urchins at least, long-lived species like Strongylocentrotus franciscanus and medium-lived ones like Strongylocentrotus purpuratus have short telomere lengths of around 5 kb, while short-lived species like Lytechinus variegatus have long telomeres of around 20 kb. Nevertheless, no telomere shortening takes place in any of these three examples.

And the telomere length of the Chrysemys picta painted turtle is over 60 kb. Apparently, this length and its subsequent growth rate is maintained with age. The related Emys orbicularis European freshwater turtle doesnt show any signs of senescence according to current knowledge. The latter maintains its 20 kb telomeres constant with age.

Q: Does the precise telomeric sequence vary among species?

A: Yes, major groups of animal species contain different telomeric sequences as follows.

The vertebrate (TTAGGG)n telomeric repeat sequence is common in most multicellular organisms, including:

Exceptions include roundworms and arthropods. The nematode telomere motif is (TTAGGC)n, while the arthropod telomere motif is (TTAGG)n. Beetles lost the arthropod telomere motif and likely employ alternative lengthening of telomere elongation.

Q: Does telomerase cause cancer?

A: According to the telomere loss theory, telomere shortening leads to the aging of cells and that of the whole organism and presumably, this phenomenon evolved to protect us from cells replicating to their hearts content and giving us cancer in exchange.

Telomeres shorten with age and that leads to replicative senescence. Making these somatic cells express telomerase is desirable for allaying many degenerative processes, but the greatest fear is that such a process may lead to the onset of cancer.

Here are two reasons for which this is an unfounded fear:

Q: Does telomerase increase lifespan?

A: Not exactly. Telomerase expression seems to correlate with the regenerative potential of a species or at least that of its germ and stem cells and not so much with its maximum lifespan.

In one experiment, telomerase was inserted in adult and old mice with the help of a viral vector. A life extension of 24 % in the adults and 13 % in the elderly was achieved. And compared to controls, the treated mice did not develop cancer at a higher rate.

But several species express telomerase in their somatic cells when indeterminate growth and/or vegetative reproduction is at play and yet, several cases of aging can be encountered in there as well.

In another experiment previously cited as well 3 species of sea urchins express telomerase in their cells and yet, their wildly differing lifespans include:

Telomerase is present in the early and adult stages of all these sea urchins and their telomere lengths show no age-related shortening. So telomere length is not the mechanism underlying their lifespan differences. And there is no difference in oxidative damage between them. All of the previously mentioned sea urchins maintain regeneration abilities with age. Go figure. Can you solve this puzzle? Can you explain why do these types of urchins have wildly different lifespans when they start out with all the cards in their favor? Id love to hear from you in a comment!

To wrap things up, I view telomerase insertion in somatic cells as paving the way for regenerative medicine to do wonders in acute and chronic diseases of the aged, but I doubt it could impact human lifespan other than by alleviating what cant be alleviated today.

Cited studies include:

Francis, N., T. Gregg, R. Owen, T. Ebert, and A. Bodnar. Lack of Age-associated Telomere Shortening in Long- and Short-lived Species of Sea Urchins. FEBS Letters580, no. 19 (August 2006): 4713-7. doi:10.1016/j.febslet.2006.07.049

Gomes, N.M., J.W. Shay, and W.E. Wright. Telomere Biology in Metazoa. FEBS Lett 584, no. 17 (September 2010): 3741-3751. doi:10.1016/j.febslet.2010.07.031.

De Jesus, B., E. Vera, K. Schneeberger, AM Tejera, E. Ayuso, F. Bosch, and MA Blasco. Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer. EMBO Mol Med 4, no. 8 (August 2012): 691-704. doi:10.1002/emmm.201200245.

Note: this blog post includes excerpts from The aging gap between species book.

Anca Iovi is the author of Eat Less Live Longer: Your Practical Guide to Calorie Restriction with Optimal Nutrition ,The Aging Gap Between Species and What Is Your Legacy? 101Ways on Getting Started to Create and Build One available on Amazon and several other places. If you enjoyed this article, dont forget to sign up to receive updates on longevity news and novel book projects!

Dont miss out on the Pinterest board on calorie restriction with optimal nutrition where she uploads new recipes every day. https://www.pinterest.com/longevityletter/eat-less-live-longer/Or the Comparative Gerontology Facebook Group where you can join the discussions on how species rate at different speeds and what could be the mechanisms underlining these differences! https://www.facebook.com/groups/683953735071847/

The dose makes the poison.

In large doses, a stressor can kill you. In low doses, it can make you stronger. The specific adaptation that a cell derives from being exposed to a low dose of some stressor is called hormesis. And this concept is central to understanding aging.

Because if cells for whatever reason lack what they need, autophagy sets in and they often survive. Autophagy or self-eating is the process through which a cell recycles its own intercellular junk and damaged organelles in order to get the building blocks it needs to continue living. Unfortunately, the ability of a cell to undergo autophagy in response to stress declines with age. That is why you must avoid the buildup of intracellular junk as much as possible and if possible, train the ability to undergo autophagy.And this is exactly what you will learn from this blog post.

Here are 3 simple things you must do to initiate autophagy and stop the aging clock:

I admit I am not a sports buff. Worse than this, I hated sport during my school years because it took me away from reading books and frankly, I found it boring and useless. Things only began to change once I learned how to swim at the mathusalemic age of 25. I now swim 1-2 times per week and I still view it as the best sport ever. I used to ride a bike during my college years, but Bucharest is not a bike-friendly place so I ended up giving away my bike and renting one out when Im in the mood for it.

But after reading Stop the clock the optimal anti-aging strategy by P.D. Mangan, I realized that I was doing it all wrong. When compared to aerobic exercise, weightlifting and high-intensity exercise training are better options to stress the body and induce autophagy. Of course, this wont make me give up swimming, but now I wont hesitate to catch the subway if the situation calls for it. And the subway always seems to be arriving when its too late for me to catch it. Murphys law.

I wish all mothers of grown-up kids would read this. Skipping eating for more than the usual 8-hour night fast is not the end of the world. It wont kill you. Better still, fasting will activate autophagy. As your cells sense they lack nutrients, they will start recycling whatever intracellular junk you accumulated. In Stop the clock the optimal anti-aging strategy, the author recommends fasts of 12-16 hours including the 8-hour fast. That could be achieved by skipping breakfast and dinner from time to time. And in my case, thats often what I do during hectic days.

Plants are literally rooted in the ground, so the only way they can protect themselves from being eaten is chemical warfare. They cant shade themselves from the sun and they cant run away to save their lives like animals do so they synthesize all sorts of toxins and pigments. This may be the reason for their purported health benefits. Personally, I never really liked meat until I discovered sushi during college , but Ive always loved colors; a plate full of veggies and/or fruits looks so beautiful. Its nice to know that having an eye for color turns out to be another simple way to initiate autophagy. And many phytochemicals like anthocyanins, resveratrol, curcumin can be ingested from veggies, fruits, herbs, tea, coffee, chocolate (the real one!) and/or dietary supplements.

And while I wholeheartedly agree with most of the advice given inStop the clock the optimal anti-aging strategy, I dont condone the low-carb paleo diet as being efficient on the long term. The moment youll lower your carbs, you will by default ingest more fats and more protein. And the body can definitely use fats and proteins to get you some energy, but it takes time to mostly complete your glycogen stores. Not to mention that half of the effect of calorie restriction is protein or more exactly methionine restriction. Paleo diets with no sugar, grains or oils sound very good in theory, but in practice people will replace them with lots of daily animal products. I personally find the paleo diet slows me down both mentally and physically. I need carbs to move fast and think fast. But if you found success by trying paleo, good for you!

Summing up, the dose makes the poison. And this is true for the 3 simple steps mentioned above too.

Most life extension animal studies stressed those animals at a bearable limit by using all sorts of stressors: calorie restriction, cold, toxins and many others. And the common denominator in all these studies is the inhibition of growth which is a positive thing after the maturity stage has been achieved.

Nevertheless, species in the wild often adapt to nutrient-poor, water-poor and oxygen-poor environments by varying the age at which maturation takes place and by varying the degree of necessary maturation. In other words, such species may either delay their maturation age (the tiny Arctica islandica clam needs 10 years to become an adult) or they may undergo reproductive system maturation only. The latter is the case of neotenic amphibians that forgo the costly metamorphosis and preserve their youthful appearance (the Proteus anguinus olm). These are evolutionarily conserved mechanisms that inhibit growth and cell division stimulating hormones like insulin and thyroid hormones.

But since most of you reading this post already finished growing up, the lesson is simple: comfort is your enemy.

(Hint: if you want to read this book, you can check it out on Amazon)

Anca Iovi is the author of Eat Less Live Longer: Your Practical Guide to Calorie Restriction with Optimal Nutrition ,The Aging Gap Between Species and What Is Your Legacy? 101Ways on Getting Started to Create and Build One available on Amazon and several other places. If you enjoyed this article, dont forget to sign up to receive updates on longevity news and novel book projects!

Dont miss out on the Pinterest board on calorie restriction with optimal nutrition where she uploads new recipes every day. https://www.pinterest.com/longevityletter/eat-less-live-longer/ Or the Comparative Gerontology Facebook Group where you can join the discussions on how species rate at different speeds and what could be the mechanisms underlining these differences! https://www.facebook.com/groups/683953735071847/

Books

Although physicians have better technologies today to uproot cancer from the human body, receiving a diagnosis of cancer is still a very stressful ordeal, even when it is cured in the end or even when the tumor is not proved to be malignant in the first place!

Lifestyle is important in preventing cancer, but at the end of the day, there is only so much you can do. I mean, humans still have a 33% chance of developing cancer during their lifespan just because they are humans.

But thats not the case in all animal species. Unfortunately, when it comes to oncology research, very few types of animals are studied to help us find treatments. Mice have an 80% rate of developing cancer if raised in a lab. They live about 2 years in the wild, so they dont need to worry about the possibility of developing cancer. But nature develops all sorts of evolutionary experiments and when it comes to cancer, here are 10 of them:

1 The naked mole rat is a rodent species where no individual was ever found of developing tumors. Even if tumors are discovered in the near future, its rarity is a mystery for a rodent the size of an average mouse. One mechanism supporting this increased cell contact inhibition of the average naked mole rat is their constituent hyaluronan, which has a molecular weight 5 times larger than ours. It sure helps that growth is expensive in their environment and they developed an uncanny ability to survive prolonged periods of starvation and intermittent oxygen restriction.

2 The smaller and shorter-lived the animal, the easier and cheaper it is to study it in the lab. The problem with this approach is that the more cells an animal has and the longer one lives, thereby surviving more cell divisions, the higher the chance of an animal should be to develop cancer, right? Only that its wrong! Known as the Petos paradox, larger animals actually have a decreased rate of cancer throughout their lifespan. One such interesting animal is the bowhead whale which is the longest-lived mammal surviving up to 2 centuries. Although hunted by humans for food apart from rivaling killer whales cancer is almost never found in these giant sea lords who are just as accustomed to prolonged starvation and intermittent oxygen restriction (during diving for feeding) as naked mole rats.

3 Another animal of considerable size with very few cases of cancer is the elephant. Now bigger animals have cells with bigger cell diameters as well. But when it comes to weighing several tonnes, the elephant living around 70 years in the wild must be an evolutionary experiment as well since cancers are so rare. One recent explanation could be the sheer number of copies of the p53 gene compared to healthy humans who have only 2 or cancer-prone Li-Fraumeni syndrome who have only 1 copy.

4 One of the mechanisms larger animals learned to keep cancer at bay was to turn off telomerase in their somatic cells. Certainly, telomerase is an enzyme present in most human cancer cells that allows them to escape normal limits on growth and become immortal. But although telomerase suppression is present in many longer-lived species, I doubt it does them any good as it stops regeneration in its tracks and it increases genomic instability. In other words, somatic telomerase repression could be a side effect and not necessarily a desired effect. And the way to check for that is to study species that dont bother with it what are their usual cancer rates? Youd expect that an animal with indeterminate growth that avoid somatic telomerase suppression to have at least an average if not higher cancer rate, right? Well the red sea urchin certainly does not. Although living close to a century, its cancer rate is close to zero.

5 You may think that the red sea urchin and many of its sea urchin relatives are rarely studied, so thats why its cancer rate is so low. But take lobsters these are commercially important species that cater to most peoples plates. The average lobster leads a benthic lifestyle as well, living at the bottom of the water and being exposed to many carcinogens. And the average lobster goes on growing for the rest of its life. And yet its cancer rate is extremely low.

6 Decapod crustaceans in general are useful biological models in oncology research because they display indeterminate growth and rarely get cancer. Apart from lobsters, these include crabs, shrimp and crayfish.

7 One small rodent that displays abundant telomerase in its tissues is the gray squirrel and yet when it comes to placing its cells in a culture dish, their spontaneous proliferation is extremely slow. Go figure.

8 The axolotl is a frequently used animal in regenerative medicine studies, but rarely used in oncology research even if its cancer rate is low.

9 A group of species in which the cancer rate is surprisingly low is formed of long-lived seabirds.

10 Another rodent with cancer-proofing strategies is the blind mole rat. Living underground just like the naked mole rat, this rodent has a double set of interferon genes which may kill cancer cells in the first place.

Classical cancer studies were extremely helpful in developing chemoterapy, novel cancer surgery techniques, radiotherapy and hormone blockers, but whats the next step? Can we do better than this? Can we adopt genetic strategies from animal species that learned how to prevent cancer in the first place?

References

Most references were taken from the Cancer chapter in The aging gap between species.

Dang, CV. A metabolic perspective of Petos paradox and cancer. Philos Trans R Soc Lond B Biol Sci 370, no. 1673 (July 2015). doi:10.1098/rstb.2014.0223.

Gomes, N.M., J.W. Shay, and W.E. Wright. Telomere Biology in Metazoa. FEBS Lett 584, no. 17 (September 2010): 3741-3751. doi:10.1016/j.febslet.2010.07.031.

Gorbunova, V., A. Seluanov, Z. Zhang, VN Gladyshev, and J. Vijg. Comparative genetics of longevity and cancer: insights from long-lived rodents. Nat Rev Genet 15, no. 8 (August 2014): 531-40. doi:10.1038/nrg3728.

Maciak, S., and P. Michalak. Cell size and cancer: a new solution to Petos paradox? Evolutionary applications 8, no. 1 (January 2015): 2-8. doi:10.1111/eva.12228.

Nagy, J.D., E.M. Victor, and J.H. Cropper. Why dont all whales have cancer? A novel hypothesis resolving Petos paradox. Integrative and Comparative Biology 47, no. 2 (August 2007): 317-28. doi:10.1093/icb/icm062.

Prokopov, A.F. Theoretical paper: exploring overlooked natural mitochondria-rejuvenative intervention: the puzzle of bowhead whales and naked mole rats. Rejuvenation Research 10, no. 4 (December 2007): 543-60. doi:10.1089/rej.2007.0546.

Roy, S., and S. Gatien. Regeneration in Axolotls: a Model to Aim For! Exp Gerontol 43, no. 11 (November 2008): 968-973. doi:10.1016/j.exger.2008.09.003.

Abegglen LM, Caulin AF, Chan A, et al. Potential Mechanisms for Cancer Resistance in Elephants and Comparative Cellular Response to DNA Damage in Humans. JAMA. 2015;314(17):1850-1860. doi:10.1001/jama.2015.13134.

Anca Iovi is the author of Eat Less Live Longer: Your Practical Guide to Calorie Restriction with Optimal Nutrition ,The Aging Gap Between Species and What Is Your Legacy? 101Ways on Getting Started to Create and Build One available on Amazon and several other places. If you enjoyed this article, dont forget to sign up to receive updates on longevity news and novel book projects!

Dont miss out on the Pinterest board on calorie restriction with optimal nutrition where she uploads new recipes every day. https://www.pinterest.com/longevityletter/eat-less-live-longer/ Or the Comparative Gerontology Facebook Group where you can join the discussions on how species rate at different speeds and what could be the mechanisms underlining these differences! https://www.facebook.com/groups/683953735071847/

Publication Year: 2015 ISBN: 9781517484811

Continued here:
Longevity Letter | Aging is a natural disease, but a ...

Nature has cures for all diseases. In Cure the Incurable the author suggests some successful alternative treatments of diseases written off by traditional medicine as incurable.

One book that has already changed thousands of lives. Let it change yours too!

Mikhail Tombak, Ph.D. graduated from the faculty of biology and chemistry of the Russian University. For many years he was the head of Center for Health Sciences in Moscow; also the author of several bestsellers on the subject of health and healing.

Much has been written lately about ways to attain long and healthy life. Numerous miracle diets are presented, formulas are praised for their extraordinary qualities, weight-reduction and aging-reversal methods are advertised. People are led to believe that good health may be the result of taking a miraculous pill. In reality, return to full health requires many years of effort, just as our diseases are caused by many years of neglect.Full health does not depend on miraculous medication and formulas that cause weight loss or aging reversal, but on the lifestyle that is in harmony with nature. This philosophy permeates the contents of this book. The author, Mikhail Tombak, created a holistic system of maintaining good health.

Before you medicate, educate yourself!

The book does not contain miraculous diets; it contains simple principles for maintaining andprotecting our health. There is no requirement of strict calorie counting but there are simple, obvious, and natural nutritional principles. The author emphasizes close connection between our health and the way we eat, breathe, and take care of all our physical and psychological needs. The question is not limited to nutrition onlyas is the case with many dieting programs.

This book is intended to be a practical health maintenance guide. If you feel that your health has begun deteriorating, waste no time - start acting quickly and take better care of yourself. The sooner you start acting the speedier your health will be restored! It is important to make gradual lifestyle changes and allow your body enough time for adjustment.

This toolbox of simple guidelines enables thousands of readers every day to live healthier, and more fulfilling lives. Let this book be your guide to anti aging, longevity, vibrant health, and overall wellbeing.

Buy "Can We Live 150 years?" and "Cure the Incurable"now!

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Mikail Tombak's books are available in the following languages:

Can We Live 150 years? is available in:

Polish- Czy Mozna Zyc 150 lat? Spanish- Podemos vivir 150 aos? Romanian- Cum sa traim 150 de ani Korean -150 ? Czech -Je mon t 150 let? Norwegian - Lev lenger German - Knnen wir 150 Jahre alt werden? Turkish - 150 yl yaayabiliriz Lithuanian- Kaip sveikai gyventi 150 met

Cure the Incurable is available in:

Polish- Uleczyc Nieuleczalne Czech- Vylit nevyliteln Romanian- Vindecarea bolilor incurabile prin metode naturale Turkish iyilemeyecek hastalk yoktur Lithuanian-Pagydyti nepagydom German in translation

"The doctor of the future will give no medicine, but will interest his patient in the care of the human frame, in diet, and in the cause and prevention of disease." Thomas Edison

Disclaimer: The information on this website is presented for educational purposes only and it is not intended to diagnose, treat, cure, or prevent any disease. Nothing listed on this website should be considered as medical advice for dealing with a given problem. You should consult your health care professional for individual guidance for specific health problems.

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Guthrie ... production assistant: Rhombus Media (as David Guthrie) Rhonda Hall ... stand-in: Canada Ginette Hamel ... on-set physiotherapist: Canada Nigel Hartwell ... production assistant Edwin Hawkeswood ... set production assistant: Canada (as Eddie Hawkeswood) Michael Healey ... adr loop group John Hirata ... stand-in: Uruguay Ryan Hollyman ... adr loop group Elise Hori ... stand-in: Brazil Daniel Horvat ... key production accountant Yuka Hoshino ... marketing executive: GAGA Communications Rogrio Jacyntino ... production secretary: Brazil & Uruguay John Jarvis ... adr loop group Winnifred Jong ... script supervisor Dbora Kaganovicius ... unit production assistant: Uruguay (as Deborah Kaganovicius) Ronan Keane ... first assistant accountant payroll: Canada Kathy Kerrin ... accountant: Bee Vine Pictures Joanna King ... office and distribution coordinator: Rhombus Media Takahiro Kobayashi ... legal consultant: IFF/CINV Toshio Kondo ... advisor: Bee Vine Pictures Alex Kontsalakis ... first assistant accountant: Canada Kevin Krikst ... assistant: Niv Fichman, Rhombus Media Mary Krohnert ... adr loop group Pablo Laporte De Armas ... unit production assistant: Uruguay Esli Leal ... financial coordinator: 02 Filmes Fernanda Leite ... assistant location manager: Brazil Joo Leite ... roadie Joao Mauricio Leonel ... set assistant: Brazil Erika Levi ... personal assistant: Uruguay George P. Lin ... accountant: Bee Vine Pictures (as George Lin) Simone Lindo ... second accounting assistant: Canada (as Simone J. Lindo) Leonardo Luppi ... stand-in: Uruguay Kate Lynch ... adr loop group Eduardo Lyon ... assistant: Fernando Meirelles, 02 Filmes Santiago Lpez ... assistant location manager: Uruguay Maria Victoria Mach Bengor ... second unit production assistant: Uruguay Maria Leticia Macorin ... location manager trainee: Brazil Lilit 'Hank' Malins ... location manager: Canada Nozomi Masuka ... script translator: Japan Hiroyuki Matsunaga ... executive assistant: Mr. Yoda, T.Y.Limited Yuka Matsushima ... financial affairs: IFF/CINV Tsuyoshi Matsushita ... promotion director: GAGA Communications Adam Meaden ... location support Marina Medeiros ... assistant acting coach: blindness, Brazil & Uruguay Murilo Meola ... stand-in: Brazil Rafal Mickiewicz ... stand-in: Canada Luiza Morandini ... personal assistant: Brazil Pedro Morelli ... assistant acting coach: blindness Mitsuya Morita ... director of business affairs: IFF/CINV Akiko Nagayo ... financial affairs: IFF/CINV Cludia Nazar ... administrative coordinator: 02 Filmes Kasumi Nishi ... legal consultant: IFF/CINV Amanda Nunes Lima ... first assistant accountant: Brazil & Uruguay Satomi Odake ... business coordinator: GAGA Communications Vital Pasquale ... assistant title designer Thoms Douglas Pastn ... production runner: 02 Filmes Maren Pedrozo ... stand-in: Uruguay Valentina Peirano ... second assistant accountant: Uruguay Josy Peres ... personal assistants coordinator: Brazil & Uruguay Shannon Perreault ... adr loop group Trina Petrik ... craft service: Canada Mimma Petrovic ... reference research: photographs Jordan Pettle ... adr loop group Joaquin P. Peyrou ... assistant location manager: Uruguay Ins Peagaricano ... location manager: Uruguay (as Ines Peagaricano) Pablo Pen ... set manager: Uruguay Henrique Pires ... reference researcher: 02 Filmes Mariana Prado ... personal assistant: Brazil Tina Marie Remedios ... production accountant Maria Helena Reneiro ... craft service: Brazil Jos Carlos Riscala ... production runner: 02 Filmes Brenda Robins ... adr loop group Gabriel Rodrigeuz Puig ... production coordinator: Uruguay Alvaro Rodrguez ... stand-in: Uruguay Ryan Rogerson ... adr loop group Alexandre Rossi ... animal wrangler: Brazil & Uruguay Richard Rotter ... production assistant: Canada Jim Russell ... legal services Stephen L. Saltzman ... legal services (as Steven Saltzman) Fernanda Sanjurjo Olavarra ... personal assistant: Uruguay Masayuki Sano ... business coordinator: Asmik Ace Entertainment Carolina Sastre ... unit production assistant: Uruguay Rafaeda Schmidt ... unit production trainee: Brazil Ed Segeren ... technical consultant Fabiana Sequeiros ... stand-in: Uruguay Emma Sereny-Johnson ... production assistant: Canada Giannina Settin ... personal assistant: Uruguay Takashi Shinomiya ... legal consultant: IFF/CINV Skye Siriunrs ... set medic: Canada Victoria Snow ... adr loop group Karie Snyder ... production secretary: Canada Darryl Stawychny ... production assistant David Storch ... adr loop group Dominic Stubbs ... accountant: Rhombus Media Alan Sutton ... fire safety coordinator Tomoyuki Suzuki ... legal consultant: IFF/CINV Kei Takahashi ... business coordinator: Asmik Ace Entertainment Charles Taylor ... firearms wrangler: Canada Drew Taylor ... location assistant: Canada Hironori Terashima ... executive business coordinator: Asmik Ace Entertainment Masao Teshima ... corporate executive: Asmik Ace Entertainment Mauro Theodoro ... stand-in: Brazil Fernando Tiezzi ... assistant blindness coach: Brazil Guillermo Daniel M. Troha ... assistant location manager: Uruguay Adrian Truss ... adr loop group Martin Ubillos ... second unit production assistant: Uruguay Yasuhide Uno ... corporate executive: GAGA Communications Milagros Uria Strauch ... assistant unit production secretary: Uruguay Mirella Valente ... assistant location manager: Brazil Laura Varela Mller ... unit production assistant: Uruguay Dolores Vargas ... second assistant accountant: Uruguay Bruno Vecchi Ricci ... production runner: 02 Filmes Al Vrkljan ... firearms wrangler: Canada (as Alan Vrkljan) Masazumi Watanabe ... director of creative affairs: IFF/CINV Wendy Williamson ... assistant production coordinator: Canada Sherry Wolfson ... travel assistant Fernando Hitoshi Yagyu ... production runner: 02 Filmes Michiko Yamaguchi ... business coordinator: GAGA Communications Celso Yamashita ... blindness coach: Brazil & Uruguay Kazuya Yamashita ... business affairs: Filosophia Mandela Youga ... craft service: Brazil Marcelo Yuar ... stand-in: Brazil Mara Zanocchi ... location manager: Uruguay (as Maria Zanocchi) Phillip Zelante ... first assistant set manager: Brazil Ricardo Zrnini ... assistant animal wrangler: Brazil & Uruguay Lucas Kater ... set assistant: Brazil (uncredited) Vanessa King ... assistant to ms. moore (uncredited)

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Blindness (2008) - Full Cast & Crew - IMDb

Change blindness is a surprising perceptual phenomenon that occurs when a change in a visual stimulus is introduced and the observer does not notice it. For example, observers often fail to notice major differences introduced into an image while it flickers off and on again.[1] People's poor ability to detect changes has been argued to reflect fundamental limitations of human attention. Change blindness has become a highly researched topic and some have argued that it may have important practical implications in areas such as eyewitness testimony and distractions while driving.

Outside of the domain of psychology, phenomena related to change blindness have been discussed since the 19th century.[2] When film editing was introduced in movies, editors began to notice that changes to the background were not noticed by those watching the film.[2] Going back much earlier, William James (18421910) was the first to mention the lack of ability to detect change in his book Principles of Psychology. (1890) [2]

Research on change blindness developed from investigation in other phenomena such as eye movements and working memory.[2] Although individuals have a very good memory as to whether or not they have seen an image, they are generally poor at recalling the smaller details in that image.[3][4] When we are visually stimulated with a complex picture, it is more likely that individuals retain only a gist of an image and not the image in its entirety.

The laboratory study of change blindness began in the 1970s within the context of eye movement research. McConkie conducted the first studies on change blindness involving changes in words and texts; in these studies, the changes were introduced while the observer performed a saccadic eye movement. Observers often failed to notice these changes.[5]

In the late 1980s, the first clear experimental demonstration was published showing very poor change detection in complex displays over brief intervals without eye movements being involved. Pashler (1988) showed that observers were poor at detecting changes introduced into arrays of letters while the display was flickered off and on, even if the offset was as brief as 67 milliseconds (although offsets briefer than that produced much more effective change detection). Pashler concluded by noting how odd it was that people generally report having a "clear sense of apprehending the identities and locations of large numbers of objects in a scene" (p.377), and that given this introspective sense, it seemed quite surprising how poor is their detection of changes.[2]

With the rise of the ability to present complex, real-world images on a computer screen, Dr. George McConkie, in the early 1990s, as part of the new initiatives of the new Beckman Institute for Advanced Science and Technology, began a renewed attempt to investigate why the world looked stable and continuous despite the shifting retinal input signal that accompanied each saccade.[6][7] This research began when John Grimes and Dr. George McConkie (1996) began to use actual photographs to study visual stability.[8] This development in change blindness research was able to show the effects of change blindness in more realistic settings.[9] Additionally, further research stated that rather large changes will not be detected when they occur during saccadic movements of the eye. In the first experiment of this kind, in 1995, Blackmore et al forced saccades by moving the image and making a change in the scene at the same time.[10] Observers ability to detect the changes fell to chance. The effect was stronger using this method than when using brief grey flashes between images, although subsequent research has mostly used grey flashes or masking stimuli. Another finding based on similar studies stated that a change was easily picked up on by participants when the eye was fixated on the point of change. Therefore, the eye must be directly fixated on the area of change for it to be noticed. This was called the saccade target theory of transsaccadic memory of visual stability.[6][7][11] However, other research in the mid-1990s has indicated that individuals still have difficulty detecting change even when they are directly fixated on a particular scene. A study by Rensink, ORegan, & Clarke demonstrated that change blindness can have an effect even if the eye was fixated on a scene. In this study, a picture was presented followed by a blank screen or masking stimulus, which was followed by the initial picture with a change. The masking stimulus almost acts like a saccadic movement of the eye which makes it significantly more difficult for individuals to detect the change.[9] This was a critical contribution to change blindness research because it demonstrated that a change can remain unnoticed with the smallest disruptions.

Research on change blindness proceeded one step further into practical applications of this phenomenon. For example, there does not have to be a masking stimulus in order for individuals to miss a change in a scene. Individuals often take significantly longer to notice certain changes if there are a few small, high contrast shapes that are temporarily splattered over a picture.[12] This method for testing change blindness is called mudsplashes.[12] This method is particularly relevant to individuals driving in a car when there is a visual obstruction on the windshield. This obstruction may impair an individuals ability to detect a change in their environment which could result in severe negative consequences while driving.

Research indicates that detecting changes in a change blindness task is easier when items are holistically processed, such as faces. Individuals notice a change faster when required to detect changes in facial features than when required to detect changes in images of houses.[13] However, individuals are better at identifying the nature of the change in houses.[13]

Other researchers have discovered that mental processing in change blindness begins even before the change is presented. More specifically, there is increased brain activity in the parietal-occipital and occipital regions prior to the emergence of a change in a change blindness task.[14]

Researchers have also indicated there is a difference in brain activity between detecting a change and identifying change in an image. Detecting a change is associated with a higher ERP (Event-related potential) whereas identifying change is associated with an increased ERP before and after the change was presented.[15]

Additional research using fluctuations in ERPs (Event-related potentials) has observed that changes in pictures (change blindness) are represented in the brain, even without the perceivers conscious awareness of the change.[16]

Lucid dreaming occurs when one realizes that the events experienced within a dream are bizarre or would not occur in ones waking life.[17] As such, the inability to notice the bizarre nature of the dream has been coined as an example of change blindness, also known as individuals who are non-lucid dreamers. However, a recent study found that lucid dreamers did not perform better on a change blindness task than non-lucid dreamers.[17] Therefore, the relation between lucid dreamers and change blindness has been discredited to some degree.

Another interesting area of research is the decreased susceptibility to change blindness when individuals are placed in teams. Although change blindness is still observed within teams, research has indicated that changes between images are noticed more when individuals work in teams as opposed to individually.[18] Both teamwork and communication assist teams in correctly identifying changes between images.[18]

Another recent study looked at the relation between expertise and change blindness. Physics experts were more likely to notice a change between two physics problems than novices.[19] It is hypothesized that experts are better at analyzing problems on a deeper level whereas novices employ a surface-level analysis. This research suggests that observing the phenomenon of change blindness may be conditional upon the context of the task.

Cognitive psychologists expanded the study of Change Blindness into decision-making. In one study, they showed participants ten pairs of faces and asked them to choose which face was more attractive. For some pairs, the experimenter used sleight of hand to show participants a face they had NOT chosen. Only 26% of subjects noticed the mismatch between their choice of face and the different face they were shown instead. The experimenters tested pairs of faces that were either high in similarity or low in similarity, but the detection rate was no different between those conditions. Subjects were also asked to give reasons why they had chosen a face (although due to the sleight of hand they actually hadn't chosen it). Despite the mismatch, subjects gave responses that were comparable in emotionality, specificity, and certainty for faces they had or had not actually chosen.[20] Further research has showed that the failure to detect mismatches between intention and outcome exists in consumer product choices [21] and in political attitudes.[22]

This method was used in the first, 1995, experiment. A change is made in an image at the same time as the image is moved in an unpredictable direction, forcing a saccade. This method mimics eye movements and can detect change blindness without introducing blank screens, masking stimuli or mudsplashes.[10]

In this paradigm, an image and an altered image are switched back and forth with a blank screen in the middle.[1] This procedure is performed at a very high rate and observers are told to click a button as soon as they see the difference between the two images.[1] This method of studying change blindness has helped researchers discover two very important findings. The first finding is that it usually takes a while for individuals to notice a change even though they are being instructed to search for a change.[1] In some cases, it can even take individuals over one minute of constant flickers to determine the location of the change. The second important finding is that changes towards the middle of a picture are noticed at a faster rate than changes on the side of a picture.[1] Although the flicker paradigm was first used in the late 1990s, it is still commonly used in current research on change blindness and has contributed to current knowledge on change blindness.

Individuals who are tested under the forced choice paradigm are only allowed to view the two pictures once before they make a choice.[9] Both images are also shown for the same amount of time.[9] The flicker paradigm and the forced choice detection paradigm are known as intentional change detection tasks, which means that the participants know they are trying to detect change. These studies have shown that even while participants are focusing their attention and searching for a change, the change may remain unnoticed.

Mudsplashes are small, high contrast shapes that are scattered over an image, but do not cover the area of the picture in which the change occurs. This mudsplash effect prevents individuals from noticing the change between the two pictures.[12] A practical application of this paradigm is that dangerous stimuli in a scene may not be noticed if there are slight obstructions in an individual's visual field. Previously, it has been stated that humans hold a very good internal representation of visual stimuli. Studies involving mudsplashes have shown that change blindness may occur because our internal representations of visual stimuli may be much worse than previous studies have shown.[12] Mudsplashes have not been used as frequently as the flicker or forced choice detection paradigms in change blindness research, but have yielded many significant and groundbreaking results.

The foreground-background segregation method for studying change blindness uses photographs of scenery with a distinct foreground and background. Researchers using this paradigm have found that individuals are usually able to recognize relatively small changes in the foreground of an image.[23] In addition, large changes to the colour of the background take significantly longer to detect.[23] This paradigm is critical to change blindness research because many previous studies have not examined the location of changes in the visual field.

Various studies have used MRIs (Magnetic Resonance Imaging) to measure brain activity when individuals detect (or fail to detect) a change in the environment. When individuals detect a change, the neural networks of the parietal and right dorsolateral prefrontal lobe regions are strongly activated.[24][25] If individuals were instructed to detect changes in faces, the fusiform face area was also significantly activated. In addition, other structures such as the pulvinar, cerebellum, and inferior temporal gyrus also showed an increase in activation when individuals reported a change.[25] It has been proposed that the parietal and frontal cortex along with the cerebellum and pulvinar might be used to direct an organisms attention to a change in the environment. A decrease of activation in these brain areas was observed if a change was not detected by the organism.[24] Furthermore, the neurological activation of these highlighted brain areas was correlated with an individuals conscious awareness of change and not the physical change itself.[25]

Other studies using fMRI (Functional Magnetic Resonance Imaging) scanners have shown that when change is not consciously detected, there was a significant decrease in the dorsolateral prefrontal and parietal lobe regions.[24] These results further the importance of the dorsolateral prefrontal and parietal cortext in the detection of visual change. In addition to fMRI studies, recent research has used transcranial magnetic stimulation (TMS) in order to inhibit areas of the brain while participants were instructed to try to detect the change between two images.[26] The results show that when the posterior parietal cortex (PPC) is inhibited, individuals are significantly slower at detecting change.[26] The PPC is critical for encoding and maintaining visual images in short term working memory, which demonstrates the importance of the PPC in terms of detecting changes between images.[26] For a change to be detected, the information of the first picture needs to be held in working memory and compared to the second picture. If the PPC is inhibited, the area of the brain responsible for encoding visual images will not function properly. The information will not be encoded and will not be held in working memory and compared to the second picture, thus inducing change blindness.

The role of attention is critical for an organisms ability to detect change. In order for an organism to detect change, visual stimulation must enter through eye and proceed through the visual stream in the brain. A study in 2004 demonstrated that if the superior colliculus (responsible for eye movements) of a monkeys brain is electrically stimulated, there would be a significant decrease in reaction time to detect the change.[27] Therefore, it is critical for organisms to attend to the change in order for it to be detected. Organisms are only able to detect this change once the visual stimulation comes through the eye (its movements are controlled by the superior colliculus) and is subsequently processed through the visual stream.

Age has been implicated as one of the factors which modulates the severity of change blindness. In a study conducted by Veiel et al. it was found that older individuals were slower to detect the changes in a change blindness experiment than were younger individuals.[28] This trend was also noticed by Caird et al., who found that drivers aged 65 and older were more prone to making incorrect decisions after a change blindness paradigm was used at an intersection, than were participants aged 1864.[29]

Attention is another factor that has been implicated in change blindness. Increasing shifts in attention decrease the severity of change blindness[30] and changes in the foreground are detected more readily than changes made to the background of an image, an effect of the intentional bias for foreground elements.[31]

Object presentation is the way in which objects appear and is a factor that determines the occurrence of change blindness. Change blindness can occur even without a delay between the original image and the altered image, but only if the change in the image forces the viewer to redefine the objects in the image.[32] Additionally, the appearance of a new object is more resistant to change blindness than a looming object, and both the appearance of a new object and the looming of an object are more resistant to change blindness than the receding of an object.[33] Furthermore, the appearance or onset of an object is more resistant to the occurrence of change blindness than the disappearance or offset of an object.[34]

Substance use has been found to affect the detection biases on change detection tasks. If an individual was presented with two changes simultaneously, those that had a change related to the substance they use regularly reported using the substance more than those detecting the neutral stimuli. This indicates a relationship between substance use and change detection within a change blindness paradigm.[35] This bias for devoting more attention to the drug-relevant stimuli is also observed with problem drinkers. Individuals who have a more severe drinking problem are quicker to detect changes in alcohol-related stimuli than in neutral stimuli.[36]

In addition to change blindness induced by changes in visual images, change blindness also exists for the other senses:

The phenomenon of change blindness has practical implications in the following areas:

Research in change blindness has uncovered the possibility of inaccuracy in eyewitness testimony.[39] In many cases, witnesses are rarely able to detect a change in the criminal's identity unless first intending to remember the incident in question.[39] This inability to detect a change in identity can lead to inaccuracy in identifying criminals, mistaken eyewitness identification, and wrongful conviction.[40] Therefore, eyewitness testimonies should be handled with caution in court in order to avoid any of these negative consequences.[40]

Older drivers make more incorrect decisions than younger drivers when faced with a change in the scene at an intersection.[29] This can be attributed to the fact that older individuals notice change at a slower rate compared to younger individuals.[29] In addition, the location and relevance of changes have an effect on what is noticed while driving.[41] The reaction time to changes in the driver's peripherals is much slower than the reaction time to changes that occur towards the center of the driver's visual field.[41] Furthermore, drivers are also able to recognize more relevant changes as opposed to irrelevant ones.[41] Research on the effects of change blindness while driving could provide insight into potential explanations of why car accidents occur.

Military command and control personnel who monitor multiple displays have a delayed time to accurately identify changes due to the necessity of verifying the changes, as well as the effective 'guessing' on some trials.[42] Due to the fact that control personnel have delayed reaction because of change blindness, an interface design of computer work stations may be extremely beneficial to improve the reaction time and accuracy.[42]

Change blindness blindness is defined as a misplaced confidence in ones ability to correctly identify visual changes.[43] People are fairly confident in their ability to detect a change, but most people exhibit poor performance on a change blindness task.

The spotlight effect is a social phenomenon that is defined as an overestimation of the ability of others to notice us.[45] A seemingly obvious change such as another individual changing a sweater during a memory task is rarely noticed.[45] However, the individuals switching the sweater tend to overestimate the ability of the test writers to notice the change in sweaters.[45] In the spotlight effect, this poor performance is a result of the overestimation of others ability to notice us whereas in change blindness blindness it is the overestimation of others ability to notice the sweater change. In other words, it is the distinction between noticing differences on a person and noticing differences between any images.

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Change blindness - Wikipedia, the free encyclopedia

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Floridians are increasingly feeling the effects of diabetes as thousands of people suffer from the disease, and many others may have diabetes and not know it! It is estimated that one out of every three children born after 2000 in the United States will be directly affected by diabetes.

That is why the American Diabetes Association's Southwest Florida office is committed to educating the public about how to stop diabetes and support those living with the disease.

We are here to help.

American Diabetes Month, takes place each November, it's designed to focus the nation's attention on issues surrounding diabetes and the people who are impacted. This year's theme, "Eat Well, America!" can show our nation how easy and joyful healthy eating can be. Download American Diabetes Month tools and resources for your company or organization at http://www.diabetes.org/adm.

For more information about American Diabetes Month activites in Southwest Florida, please contact our local office at 813-885-5007.

Healthy Sarasota Week We have collaborated with LECOM & the Sarasota community for the first annual Healthy Sarasota Week. Join our call to action to increase awareness by providing events for citizens and businesses to make critical healthy life changes. All Sarasota Week actives are free, please reserve your spot today!

I Decide to Stop Diabetes (ID Day) In concert with the other American Diabetes Month activities, churches across the country are engaging their communities in celebration of ID Day at Church, a nationwide movement to Stop Diabetes.

This community and faith based education programs and workshops aims to increase awareness of the rates of diabetes among African Americans. The initiative educates this audience about the seriousness of diabetes and its complications by teaching the importance of making healthy lifestyle choices and educating those with or at risk for developing diabetes about prevention and management

For more information, please contact Alisa Barksdale at abarksdale@diabetes.org.

Learning to live with diabetes does not happen overnight our message to parents and children is you don't have to do it alone. Family Link connects families with other families of kids with diabetes. Our goal is to help connect parents with mentors who understand how they are feeling, and through fun and social diabetes education events, offer families an opportunity to learn more about diabetes and meet other families of children with diabetes.

If you would like to be part of our Family Link Program, please contact Alisa Barksdale at abarksdale@diabetes.org.

The American Diabetes Association is the leading advocate for the rights of children and adults with diabetes. Children spend most of their time at school. The Association provides parents with resources and training modules to help them work with their child's school to create a medically safe learning environment for your child. Parent "Safe at School" workshops are offered twice a year.

For more information, please contact Alisa Barksdale at abarksdale@diabetes.org.

Stop Diabetes at Work is a program of the American Diabetes Association, which provides the resources for employers to use in the workplace to help employees need to live healthier liveswhether they are working to prevent diabetes or to manage diabetes if they have already been diagnosed. For more information on how to get your company involved, please click here.

We welcome your help.

Your involvement as an American Diabetes Association volunteer whether on a local or national level will help us expand our community outreach and impact, inspire healthy living, intensify our advocacy efforts, raise critical dollars to fund our mission, and uphold our reputation as the moving force and trusted leader in the diabetes community.

Find volunteer opportunities in our area through the Volunteer Center.

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The USF Diabetes Center has a dedicated team of health care professionals including pediatric and adult endocrinologists (diabetes specialists), nurse practitioners, certified diabetes educators, a clinical dietitian and a clinical psychologist. Clinical care services include:

We can educate and guide you in making those realistic lifestyle changes that can lead to improved health, help reduce your risk of complications, and can help you feel better.

The USF Diabetes Center serves as a catalyst for innovative and important research building upon active program development in clinical, basic, and transitional research. The USF Pediatric Epidemiology Center, our parent Center at USF, coordinates numerous national and international studies in diabetes and related disorders.

Having diabetes effects the entire family. Support from your loved ones can lead to successful lifestyle changes and better health for everyone. There are resources available that can help you and your family cope and successfully manage diabetes.

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Edward Gerjouy can walk briskly on an inclined treadmill for more than half an hour without too much trouble. This wouldn't be so remarkable, but for the fact that he is 92 years old.

A study in the Journal of the American Medical Association (JAMA) demonstrates that seniors like Gerjouy who can still hoof it at a relatively speedy pace have a good chance of living to an even riper old age.

When researchers at the University of Pittsburgh pooled the data from nine large studies that involved more than 34,000 seniors, they were able to correlate walking speed in people 65 or older with expected longevity.

At the beginning of each study, subjects were timed at their normal, comfortable walking pace for about 13 feet and periodically retested for up to 21 years. Anyone who could ambulate, even if they used a cane or walker, was included.

The faster an older person can walk, the longer they can expect to live and, according to the researchers, walking with some pep in your step appears to be a better predictor of who survives than simply looking at someone's age and sex.

"It's a real part of the human experience to see that when someone slows down with age, they may not be doing as well as they once were," said lead researcher Dr. Stephanie Studenski. "One of the major goals of this study was to quantify this experience for practical and clinical purposes."

Studenski notes that the act of placing one foot in front of the other requires the cooperation of many body systems including the heart, lungs, blood, bones, muscles, joints, nerves and brain -- and all of these systems synchronize, coordinate and integrate in a way that allows each individual to choose their own ideal walking speed, a speed that remains remarkably constant throughout life unless it's affected by medical issues.

For this reason, scientists consider how quickly a person walks, when correlated with age and sex, a reflection of their underlying health.

Someone like Gerjouy, for example, who at his age still strolls comfortably at about 3 miles per hour, can expect to enjoy another seven years of life. In contrast, a 75-year-old man who barely shuffles along at less than 1.0 mile per hour may not make it to his 80th birthday; and a 75-year-old woman who can keep pace with Gerjouy may look forward to celebrating another 18 birthdays.

"In fact, speed of movement seems to be linear, with each increase correlating with an increased prediction for years of life," Studenski said.

Administering a simple timed walking test could prove useful for helping doctors make more individualized healthcare recommendations. For instance, prostate cancer screening is generally considered a waste of time for men over 70 because it is widely accepted that elderly men who develop prostate cancer will most likely die of another disease or natural causes.

But if an energetic walker in his seventies can reasonably presume to live another decade in good health, he could benefit from the screening. "Functional predictions like this give doctors an opportunity to do individual life planning for healthy older people where we ought to treat them like they are going to be around for a good long time," Studenski said.

Identifying the slowpokes might help identify at-risk seniors too, so they can be targeted for interventions to help improve their health. Clinicians could even monitor speed over time as a safe and inexpensive way to red-flag slowdowns associated with developing health problems.

One caveat Studenski makes is that longevity charts are not good predictors for natural slow walkers; some healthy people simply prefer to move at a more leisurely pace.

There's little evidence to show that revving things up means living longer either, though in one previous study Studenski's team did show that people who improved walking speed over a one-year period had a better chance of survival over the following eight years compared to people who didn't speed up. And even though Studenski says there's more proof needed before it can be said that cultivating a livelier step translates to additional years, she still thinks that working on physical fitness as you age is a good idea.

"Working with your doctor, a physical therapist or some other healthcare professional to help maintain your health and your walking speed certainly can't hurt and can only help in most cases," she said.

Gerjouy jokingly attributes his good health and quick stride to a daily ration of Jell-O. Jiggly desserts aside, there are some real steps you can take to ensure you maintain mobility into your golden years. John R. Martinez a licensed physical therapist and president of Therapy Experts in New York City, offers the following tips for optimal walking.

Stay Flexible. Maintaining your flexibility, particularly in your hips, sustains your ability to move. You can stretch your hips daily by leaning forward towards your kitchen counter (usually a perfect height for this stretch) with your legs straddled a stride's distance apart. Hold for 30 seconds as you feel the stretch spread up the back of your leg into your hip. Repeat to other side.

Improve Balance. Balance is a bigger component of walking than most people realize; it's what keeps you from stumbling or tripping over your feet. For a simple daily challenge, stand on one leg while you brush your teeth. Start by hanging onto the sink with your extra hand, progress to no hands, and then to doing it with your eyes closed.

Build Endurance and Strength. As you rack up birthdays, endurance and power can diminish unless you focus on maintaining them. One way to keep up stamina is to do the very activity you are trying to preserve: Walking. This is also likely to strengthen the walking muscles too. You can mix this with lower impact endurance activities like riding a stationary bike or water exercise.

Care for Your Feet. Taking good care of your feet will ensure they remain in walk-worthy condition. Wear comfortable shoes, maintain good hygiene and visit a podiatrist periodically for a foot checkup. One easy daily foot strengthening exercise involves placing a small towel under your bare foot and scrunching it up and straightening it out with your toes. Repeat three to five times with each foot.

Lose Weight. Carrying excess weight strains your body, especially your knees, which can slow you down and prevent you from being more active. Watch your diet and do what you can to burn calories. Even a 5 percent reduction in weight can make a tremendous difference in your mobility.

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Walking Speed Predicts Longevity in Elderly - ABC News

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Integrative Family Medicine combines the practice of conventional medicine with alternative methods that focus on treating a patients mind, body and spirit. This type of medicine puts a heavy emphasis on prevention, as it is much easier to work towards preventing health issues than it is to cure them after they have occurred.

Integrative Family Medicine is most effective for patients who are motivated in self care through lifestyle changes and are therefore looking for insight on ways to do so.Our TPCA board-certifiedphysician prefers the approach of educating and coaching patients to be involved in their own treatment often using natural remedies as much as possible.

Our Integrative Family Medicine physician is ready to discuss your lifestyle and get you on the path to holistic health today. Integrative Family Medicine is available for all age groups!

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We will be moving to 1630 Riggins Rd beginning February 8th & re-open there on February 15th!! Please see the Newsletter!

There is not yet a sign for "Integrative Healthcare" on Riggins Rd. The sign for "The Arthritis Center: Szczesny John M MD" is still in place from the previous tenant.

Special Testing: We use 11+ outside labs to help find the root cause of illness. More info here

We also haveadvanced Bioimpedance for body compositionto track your body lean and fat mass as well as water balance. It is a quick test you can add to your physical exam or visit for $10 (out of pocket.)

Prolotherapyis a local injection (using a strong dextrose solution and lidocaine) which helps heal weakened joints, tendons and ligaments. These weak and partially healed areas are often the cause of chronic joint and low back pain. This is not covered by insurance please call to ask about the cost.

HeartMathtraining for stress reductionuses a small device that gives feedback on your heart rate variability. You can use this with mindfulness, deep breathing and other meditation techniques as a guide to more coherence. There is no charge if you try this during an office visit as time allows.

Elizabeth has completed several classes with the IFM institute. To see more about functional medicine, at this link for The Institute of Functional Medicine.

Our portal is for filling out registration forms, requesting appointments, and sending us questions and information in a secure and confidential manner.

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Our Staff N. Elizabeth Markovich, DNP Elizabeth completed the Masters of Science in Nursing and Family Nurse Practitioner certification in 1993 after many years as an RN. She recently completed a Doctor of Nursing Practice degree from Florida State. She has extensive experience in general family practice medicine and in rheumatology. She has a special interest in treatment of hormone imbalance, thyroid problems, reducing heart disease and diabetes risk, arthritis, and pain. She has education and experience in functional medicine, use of special testing, and working on certification with the Institute for Functional Medicine. Read more about the services Elizabeth offers in Patient Resources & News/Information Dr. John Ness, MD

Dr. Ness is our consulting physician and medical director. He is a popular local family doctor, well known for his interest in integrative medicine. He is an adjunct professor at the FSU school of medicine. He hasapractice on Universal Drive in Tallahassee and is one of the founders of the Healing Arts Alliance an organization to promote cooperation and learning among health professional interested in alternatives.

Martin Markovich is Elizabeth's husband and a partner in IHC. He has a background in business and public policy and has a PhD from RAND. He is involved in personnel and strategic planning and many other areas.

Crystal is the office manager and handles our billing. She does some in-house procedures such as venopuncture, EKG's, and nebulizer treatments. She is a certified Phlebotomist.

Erika is our anchor person at the front desk. Scheduling is her main task, taking most phone calls and routing messages. She is usually the first and last person you see in the office.

Joanna is our medical assistant. She works in the lab and is trained in phlebotomy, administers shots, nebulizer treatments and EKGs. She also takes care of referrals, patient files, faxes, Rx refills, as well as returning patient calls, assisting in reception and occasionally billing.

Please welcome our newest member to the IHC Team!! Michelle is our Office Assistant, taking over some of Joanna's responsibilities like importing documents, taking care of medical records, and checking faxes.

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Our Staff - Integrative Healthcare

Introduction

Genetics is the branch of science that deals with how you inherit physical and behavioural characteristics including medical conditions.

Your genes are a set of instructions for the growth and development of every cell in your body. For example, they determine characteristics such as your blood group and the colour of your eyes and hair.

However, many characteristics aren't due to genes alone environment also plays an important role. For example, children may inherit 'tall genes' from their parents, but if their diet doesn't provide them with the necessary nutrients, they may not grow very tall.

Genes are packaged in bundles called chromosomes. In humans, each cell in the body contains 23 pairs of chromosomes 46 in total.

You inherit one of each pair of chromosomes from your mother and one from your father. This means there are two copies of every gene in each cell, with the exception of the sex chromosomes, X and Y.

The X and Y chromosomes determine the biological sex of a baby. Babies with a Y chromosome (XY) will be male, whereas those without a Y chromosome will be female (XX). This means that males only have one copy of each X chromosome gene, rather than two, and they have a few genes found only on the Y chromosome and play an important role in male development.

Occasionally, individuals inherit more than one sex chromosome. Females with three X chromosomes (XXX) and males with an extra Y (XYY) are normal, and most never know they have an extra chromosome. However, females with one X have a condition known as Turner syndrome, and males with an extra X have Klinefelter syndrome.

The whole set of genes is known as the genome. Humans have about 21,000 genes on their 23 chromosomes, so the human genome contains two copies of those 21,000 (except for those on X and Y in males).

Deoxyribonucleic acid (DNA) is the long molecule found inside chromosomes that stores genetic information. It is tightly coiled into a double helix shape, which looks like a twisted ladder.

Each 'rung' of the ladder is made up of a combination of four chemicals adenine, thymine, cytosine and guanine which are represented as the letters A, T, C and G.

These 'letters' are ordered in particular sequences within your genes and they contain the instructions to make a particular protein, in a particular cell, at a particular time. Proteins are complex chemicals that are the building blocks of the body. For example, keratin is the protein in hair and nails, while haemoglobin is the red protein in blood.

There arearound six billion letters of DNA code within each cell.

As well as determining characteristics such as eye and hair colour, your genes can also directly cause or increase your risk of a wide range of medical conditions.

Although not always the case, many of these conditions occur when a child inherits a specific altered (mutated) version of a particular gene from one or both of their parents.

Examples of conditions directly caused by genetic mutations include:

There are also many conditions that are not directly caused by genetic mutations, but can occur as the result of a combination of an inherited genetic susceptibility and environmental factors, such as a poor diet, smoking and a lack of exercise.

Read more about how genes are inherited.

Genetic testing can be used to find out whether you are carrying a particular genetic mutation that causes a medical condition.

This can be useful for a number of purposes, including diagnosing certain genetic conditions, predicting your likelihood of developing a certain condition and determining if any children you have are at risk of developing an inherited condition.

Testing usually involves taking a blood or tissue sample and analysing the DNA in your cells.

Genetic testing can also be carried to find out if a foetus is likely to be born with a certain genetic condition by extracting and testing a sample of cells from the womb.

Read more about genetic testing and counselling.

The Human Genome Project is an international scientific project that involves thousands of scientists around the world.

The initial project ran from 1990 to 2003. Its objective was to map the immense amount of genetic information found in every human cell.

As well as identifying specific human genes, the Human Genome Project has enabled scientists to gain a better understanding of how certain traits and characteristics are passed on from parents to children.

It has also led to a better understanding of the role of genetics in a number of genetic and inherited conditions.

Page last reviewed: 08/08/2014

Next review due: 08/08/2016

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Genetics - NHS Choices

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Diabetes Mellitus Center - Richardson, TX - MedicineNet

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Texans are increasingly feeling the effects of diabetes as thousands of people suffer from the disease. Many others may have diabetes and not know it! Over 700,000 people right here in North Texas have diabetes and it's estimated that one out of every three children born after 2000 in the United States will be directly affected by diabetes.

Want to know your risk? Risk Test.

That is why the American Diabetes Association's North Texas office is so committed to educating the public about how to stop diabetes and support those living with the disease. We are here to help.

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We welcome your help.

Your involvement as an American Diabetes Association volunteer whether on a local or national level will help us expand our community outreach and impact, inspire healthy living, intensify our advocacy efforts, raise critical dollars to fund our mission, and uphold our reputation as the moving force and trusted leader in the diabetes community.

Find volunteer opportunities in our area through the Volunteer Center.

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North Texas Office of the American Diabetes Association

Type of Physician: Geneticist, Ph.D.

What is a Geneticist, Ph.D.? A certification by the Board of Medical Genetics; practitioners work in association with a medical specialist, are affiliated with a clinical genetics program, or serve as a consultant to medical and dental specialists.

Specialty: Genetics: Medical (Ph.D.)

Common Name:

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Genetic Counseling Center - Cupertino, CA - MedicineNet

First string care for every athlete

You don't have to go to an emergency room to receive care for your sports-related injury. We offer full on-site orthopedics, physical therapy and radiological services.

These are the primary phases of sports medicine that the University of Mississippi Medical Center sports medicine staff strives to fulfill when working with competitive or recreational athletes on a daily basis.

University Sports Medicine is comprised of board-certified physicians that are specialists in their chosen area and maintain faculty status with UMMC. Our physicians have developed exceptional reputations at the state, national and international levels.

The sports medicine staff has a diversity of experiences with athletes at all levels of competition. All University Sports Medicine athletic trainers are certified nationally and maintain state licensure.

The collective efforts of the physician, athletic trainer, physical therapist and others provide comprehensive medical care of the competitive or recreational athlete. University Sports Medicine is a leader in knowledge and cutting-edge techniques for sports medicine patients in Mississippi and the nation.

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University Sports Medicine - Home | University of Mississippi ...

Athletic training has been a fixture in Notre Dame athletics since the days of Knute Rockne. Notre Dames first-known athletic trainer was Eugene Scrap Iron Young, who began providing care to student-athletes in the 1920s. Athletic training continued to evolve and expand along with the Universitys athletic growth. From Youngs first days to today, Notre Dames athletic training department has developed into a fully-staffed sports medicine team with two state-of-the-art facilities.

In support of the Universitys primary goals of spiritual, intellectual and physical development of its students, the mission of the Sports Medicine Department is to fashion a program founded on integrity, accountability and scientific evidence-based doctrine.

The Sports Medicine staff will strive to provide every student-athlete with the most comprehensive, highest quality individual sports medicine health care available in a professional, efficient, compassionate and service-oriented manner.

A diversified program of prevention, evaluation, treatment and rehabilitation will assure a positive healthy recovery experience, an improved quality of life, a safe return to full athletic participation and continued athletic success.

Head athletic trainer and physical therapist Jim Russ oversees the athletic training services. The staff includes a football athlete trainer, five associate athletic trainers and nine assistant athletic trainers. The entire staff is certified by the National Athletic Trainers Association and has collectively more than 150 years of athletic training experience. Russ and his staff, along with a host of observation student athletic trainers, are responsible for the health and care of the 26 NCAA Division I sports at the University, which includes more than 750 student-athletes. Learn More about our offered Services and Testing

Each certified staff member is in charge of the health care of at least two varsity athletic teams. These responsibilities include covering practice and competition as well as traveling with the team as deemed appropriate. Specifically, the athletic trainer is responsible for evaluating and assessing athletic injuries, administering first aid and injury care, making medical referrals, and establishing treatments, rehabilitation and reconditioning of athletic injuries/illness. The athletic trainer also spends a significant amount of time in the education of student-athletes with respect to injury prevention, nutrition and psychological support in dealing with injuries. All staff athletic trainers are certified by the National Athletic Trainers Association and licensed by the state of Indiana.

The athletic training department is under the direct supervision of several sports medicine physicians. University physicians Dr. Jim Moriarity, Dr. Becky Moskwinski , Dr. Kevin McAward, Dr. Matt Leiszler, and Dr. Kathy Cahoon- serve as primary care physicians for health care needs of the student-athletes. Area orthopaedists Dr. Christopher Balint, Dr. Bob Clemency, Dr. Brian Ratigan, Dr. James Sieradski, and Dr. Mike Yergler oversee the orthopaedic needs for Irish athletes. Dr. Steve Simons oversees care of the track and field and cross country teams. The sports medicine department also utilizes the services of Dr. Jerry Hofferth as team chiropractor. Also available are a host of medical consultants to meet specific needs ranging from cardiology to dermatology. Dr. Moriarity, has earned honorary monograms from the Notre Dame Monogram Club.

The athletic training staff utilizes two state-of-the-art facilities to treat and rehabilitate injured athletes. The original athletic training room is located in the Joyce Center. The newest addition to the department is a 9,000-foot plus training facility in the state-of-the-art Loftus Athletics Training Facility which features new rehabilitation and treatment areas in addition to office space for staff.

There are alarming trends in professional-level injuries among youth sports participants. Orthopaedic surgeons see two trends: the number of youth injuries is reaching epidemic proportions and youth are experiencing overuse injuries at a younger and younger age. The high rate of youth sports injuries is fueled by an increase in overuse and trauma injuries and a lack of attention paid to proper injury prevention.

To address these issues, the American Orthopaedic Society for Sports Medicine (AOSSM) and its collaborators created the STOP Sports Injuries Campaign. Learn more at StopSportsInjuries.org

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Sports Medicine // Performance // University of Notre Dame

Our Sports Medicine Program

Florida Orthopaedic Institutes team of highly skilled sports medicine physicians and athletic trainers serve hundreds of Tampa Bay residents every week. We have the largest and most advanced sports medicine program in the region, and our surgeons are all fellowship trained in advanced arthroscopic techniques, with many years of experience.

Our sports medicine physicians have served as the team physicians for the Tampa Bay Buccaneers, Tampa Bay Lightning, Tampa Bay Storm, Tampa Bay Rowdies, University of South Florida, University of Tampa, Saint Leo University and high schools throughout Hillsborough County.

Our compassionate team of healthcare professionals uses a multidisciplinary approach to ensure the most advanced treatment for all your sports-related injuries. Just as every athlete focuses on his or her particular sport, our team is dedicated only to sports medicine, and this ensures the best possible outcome.

We understand your desire to get back into the game and will do everything we can to make it happen safely.

Our full range of our sports medicine services include:

Each year, there are between 1.6 and 3.8 million sports-related concussions in the United States. Through our partnership with ImPACT, we offer concussion screenings. To schedule a screening, please call 813-978-9797 or to learn more about ImPACT, go to: https://www.impacttest.com/about/.

Athletic trainers are the first line of defense for the prevention and evaluation of injuries during athletic activities. We offer a unique Athletic Training Outreach Program designed to keep you active. Our licensed athletic trainers provide healthcare services to athletes at practices, games, tournaments and community events in the Tampa Bay Area.

Athletic trainers are allied healthcare professionals who work with physicians on the medical staff to prevent, evaluate, manage and care for many different types of injuries.

We recognize that injuries can happen outside the typical workweek, which is we offer Saturday-morning and early afternoon clinics at our Orthopaedic Urgent Care in South Tampa. Please take advantage of this opportunity to receive medical care even if you attend a high school that is not under contract with us.

Research and education is at the forefront of the work we do. If youre interested in having one of our sports medicine physicians speak to your school group, coaching staff, or organization please contact:Donna Bossuyt, at DBossuyt@Floridaortho.com

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Sports Medicine | Florida Orthopaedic Institute

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Sports Medicine - Concussion Materials