Spiced Chocolate Cheesecake Brownie

 

Author:

Kerry Jo Brady

Serves: 2

Prep time: 5 mins

Cook time: 1 min

Total time: 6 mins

Print

 

This is so good! You have to try this!!!!

Ingredients

• Spiced Chocolate Cheesecake Brownie
• 1 packet MF Brownies
• 1 packet MF Spiced Pancakes (regular or cc. pancakes would work too)
• 1 tsp Pumpkin Pie Sugar Free Syrup (this is only ⅙ of a condiment, so I am not counting it)
• 6 TB Water
• 1 TB Cream Cheese (1 healthy fat)
• 1 packet Splenda (1 condiment)

Instructions

1. Mix together the MF Brownie and MF Spiced Pancake mixes. Add 1 teaspoon of sugar free pumpkin spiced syrup and 6 TB of water. Mix together and pour into 2 ramekins. Microwave for 1½ minutes. Take out of ramekin and let cool for about 5 minutes. Mix 1 TB of cream cheese and 1 packet of Splenda together for a topping. Divide cream cheese topping and spread evenly on top of each cake. Enjoy!

Notes

This full recipe makes 2 Medifast meals, 1 condiment & 1 healthy fat. Each cake is 1 Medifast meal, ½ condiment and ½ healthy fat serving.

3.1.09

Source:
http://get-healthier.com/spiced-chocolate-cheesecake-brownie/

Source:
http://get-healthier.com/roasted-cherry-tomatoes/

Source:
http://get-healthier.com/asian-turkey-burgers/

Source:
http://get-healthier.com/roasted-salmon-with-green-herbs/

Lorem ipsum dolor sit amet, consectetur adipisicing elit, sed do eiusmod tempor incididunt ut labore et dolore magna aliqua. Ut enim ad minim veniam, quis nostrud exercitation ullamco laboris nisi ut aliquip ex ea commodo consequat. Duis aute irure dolor in reprehenderit in voluptate velit esse cillum dolore eu fugiat nulla pariatur. Excepteur sint occaecat cupidatat non proident, sunt in culpa qui officia deserunt mollit anim id est laborum. Lorem ipsum dolor sit amet, consectetur adipisicing elit, sed do eiusmod tempor incididunt ut labore et dolore magna aliqua.

Lorem ipsum dolor sit amet, consectetur adipisicing elit, sed do eiusmod tempor incididunt ut labore et dolore magna aliqua. Ut enim ad minim veniam, quis nostrud exercitation ullamco laboris nisi ut aliquip ex ea commodo consequat. Duis aute irure dolor in reprehenderit in voluptate velit esse cillum dolore eu fugiat nulla pariatur. Excepteur sint occaecat cupidatat non proident, sunt in culpa qui officia deserunt mollit anim id est laborum. Lorem ipsum dolor sit amet, consectetur adipisicing elit, sed do eiusmod tempor incididunt ut labore et dolore magna aliqua. Ut enim ad minim veniam, quis nostrud exercitation ullamco laboris nisi ut aliquip ex ea commodo consequat. Duis aute irure dolor in reprehenderit in voluptate velit esse cillum dolore eu fugiat nulla pariatur. Excepteur sint occaecat cupidatat non proident, sunt in culpa qui officia deserunt mollit anim id est laborum. Lorem ipsum dolor sit amet, consectetur adipisicing elit, sed do eiusmod tempor incididunt ut labore et dolore magna aliqua. Ut enim ad minim veniam, quis nostrud exercitation ullamco laboris nisi ut aliquip ex ea commodo consequat.

Source:
http://get-healthier.com/this-is-an-snack-post-2/

So the future of medicine is golden, biotechnology is in the throes of a vast expansion of capabilities and free-fall in costs, and we have a good idea as to how to go about reversing aging - if the research community would just stop tinkering with efforts to merely slow down aging and get on with achieving the all-round better goal of rejuvenation. We should all donate money and time to help out, because it's not as though we can take it with us and irreplaceable time is ticking away. A shot at lifespans of centuries and longer is coming, with not so much time left in which to reach for that goal.

Putting all of that to one side for the moment, there is the arguably less important question of how to optimize heath and life span given the present poor tools to hand. Many people spend a great deal of time talking and debating on this topic, immersing themselves in the world of what presently exists, and giving little thought to what might lie ahead. A vast industry caters to people who think they've found the better mousetrap when it comes to personal health and aging. They're all wrong, of course, but that doesn't stop the flow of commerce.

The sad truth of the matter is that it's simple and easy to achieve the 80/20 result in health and longevity within the bounds of the tools we have available to us today, provided you're starting out as a basically ordinary, healthy individual. Exercise regularly, the 30 minutes daily of aerobic exercise that has been recommended by physicians since way back when, and practice calorie restriction with optimal nutrition - i.e. eat a sane diet, not very much of it, and obtain the necessary levels of micronutrients while doing so. There's also the matter of not harming yourself greatly, but just as I shouldn't have to mention avoidance of knives and falling rocks, I shouldn't have to mention things like giving up smoking.

These things are not rocket science. They are widely known and most have been advocated for centuries. The supporting statistical data is far better now than at any point in the past, and so you have no excuses: if you're not adopting these practices then it is because you have decided to accept a shorter life expectancy and greater odds of ill health in exchange for the dissipations that you presently enjoy. No-one's perfect, right?

But here is an interesting thing about trying to reliably forge ahead beyond the 80/20 point in personal health, in search of the optimum level of improvement: it's next to impossible to go further or reliably measure that you have gone further. The research community has expended billions without being able to determine how you can do that - so what makes you think that you can do any better given your far more limited resources? Metabolism and its interactions are so very, very complex. We can list with some confidence what is good for you, but talking about what is optimal is far beyond present capabilities.

For example, to pick one line item, let us consider calorie restriction. It works amazingly well in short-lived animals and improves short-term measures of human health far more than any presently available medical technology can manage. But once we get to an examination of longer lived animals (such as we primates) over the long term, it starts to become much harder to pin down the best, most optimal way to do things - certainly, the present primate studies are beginning to look as though they will generate as much ambiguity as data.

Dietary Restriction: critical cofactors to separate healthspan from lifespan benefits

Dietary restriction (DR), typically a 20-40% reduction in ad libitum or "normal" nutritional energy intake, has been reported to extend lifespan in diverse organisms including yeast, nematodes, spiders, fruit flies, mice, rats and rhesus monkeys. The magnitude of the lifespan enhancement appears to diminish with increasing organismal complexity. However, the extent of lifespan extension has been notoriously inconsistent, especially in mammals.

Recently, Mattison et al. report that DR does not extend lifespan in rhesus monkeys in contrast to earlier work of Colman et al. Examination of these papers identifies multiple potential confounding factors. Among these are the varied genetic backgrounds and composition of the "normal" and DR diets. In the monkeys, the correlation of DR with increased healthspan is stronger than that seen with lifespan, and indeed may be separable. Recent mechanistic studies in Drosophila implicate non-genetic cofactors such as level of physical activity and muscular fatty acid metabolism in the benefits of DR. These results should be followed up in mammals. Perhaps levels of physical activity among the cohorts of rhesus monkeys contributes to inconsistent DR effects.

To understand the maximum potential benefits from DR requires differentiating fundamental effects on aging at the cellular and molecular levels from suppression of age-associated diseases, such as cancer. To that end, it is important that investigators carefully evaluate the effects of DR on biomarkers of molecular aging, such as mutation rate and epigenomic alterations. Several short-term studies show that humans may benefit from DR in as little as 6 months, by achieving lowered fasting insulin levels and improved cardiovascular health.

Optimized healthspan engineering will require a much deeper understanding of DR.

That last sentence is worth considering at length - but remember that the 80/20 win for personal health is still right here, easily achieved. Instead of trying to go further in a presently impossible attempt at optimization, a better use of that time and energy lies in supporting research and development of rejuvenation biotechnology. Even a magically optimized personal health program would not allow most people to live to 100 with today's technology - the only way that the vast majority of us will get to see a three digit birthday cake is through progress in longevity science and its clinical applications.

So if you're going to spend any effort on this whole living longer in good health thing, spend it wisely. Don't chase rainbows.

Source:
http://www.fightaging.org/archives/2012/10/achieving-the-8020-point-in-general-health-is-easy-but-anything-more-is-near-impossible.php

Much like mammals, bivalve molluscs exhibit a very wide range of life spans. At the known outer end stands the arctic quahog at more than four centuries, and much studied in recent years so as to understand the roots of its longevity. That research project is still ongoing, as are similar comparative studies of aging and longevity in a range of other species.

Here, researchers compare resistance to various forms of physical stress and damage in different bivalve species. As you might expect from the view of aging put forward earlier today, longer-lived species are more resistant to most forms of damage:

Bivalve molluscs are newly discovered models of successful aging. Here, we test the hypothesis that extremely long-lived bivalves are not uniquely resistant to oxidative stressors (eg, tert-butyl hydroperoxide, as demonstrated in previous studies) but exhibit a multistress resistance phenotype.

We contrasted resistance (in terms of organismal mortality) to genotoxic stresses (including topoisomerase inhibitors, agents that cross-link DNA or impair genomic integrity through DNA alkylation or methylation) and to mitochondrial oxidative stressors in three bivalve mollusc species with dramatically differing life spans: Arctica islandica (ocean quahog), Mercenaria mercenaria (northern quahog), and the Atlantic bay scallop, Argopecten irradians irradians (maximum species life spans: more than 500, more than 100, and ~2 years, respectively).

With all stressors, the short-lived A i irradians were significantly less resistant than the two longer lived species. Arctica islandica were consistently more resistant than M mercenaria to mortality induced by oxidative stressors as well as DNA methylating agent nitrogen mustard and the DNA alkylating agent methyl methanesulfonate. The same trend was not observed for genotoxic agents that act through cross-linking DNA. In contrast, M mercenaria tended to be more resistant to epirubicin and genotoxic stressors, which cause DNA damage by inhibiting topoisomerases.

To our knowledge, this is the first study comparing resistance to genotoxic stressors in bivalve mollusc species with disparate longevities. In line with previous studies of comparative stress resistance and longevity, our data extends, at least in part, the evidence for the hypothesis that an association exists between longevity and a general resistance to multiplex stressors, not solely oxidative stress.

In mammals, you might look to the naked mole rat as an analogous species: very resistant to all sorts of biological and cellular damage, and extremely long-lived in comparison to similar sized rodent species.

Link: http://www.ncbi.nlm.nih.gov/pubmed/23051979

Source:
http://www.fightaging.org/archives/2012/10/comparing-longevity-and-damage-resistance-in-bivalves.php

Here is a framework for thinking about aging and longevity: various forms of low-level biological damage accrue as a result of the operation of metabolism, degrading organs and tissues and ultimately causing death. Where natural selection favors longer-lived individuals, mechanisms will evolve to repair, minimize, or resist the effects of this damage. So aging is driven by damage, but genetic programs interact with that damage, evolved to try to do something about it.

Thus we could expect to be able to manipulate life span either by repairing damage or by altering the programs. The former approach should produce far more effective means of healthy life extension, however, including rejuvenation of the old. In comparison, and from what we've seen so far in longevity science, modestly slowing aging is about the best we can expect from the near future of genetic and metabolic alterations.

In spite of exciting new insights into regulatory mechanisms that modulate the aging process, the proximal cause of aging remains one of the unsolved big problems in biology. An evolutionary analysis of aging provides a helpful theoretical framework by establishing boundary conditions on possible mechanisms of aging. The fundamental insight is that the force of natural selection diminishes with age. This does not preclude senescence (age-related decrease in individual fitness) from occurring in natural populations. Senescence can develop because some genes have non-separable, but typically different or opposite, functions in reproductive-age and in old individuals. Such genes, selected according to their "youthful" function, may thus impose a distinct senescent phenotype in old age.

In general, however, unless a controversial formulation of group selection is invoked, traits that would become manifest only in old age cannot evolve. This precludes the evolutionary emergence of aging programs, which have been sometimes postulated to exist in analogy to developmental and other biological programs. (By the same token, selective pressure that diminishes with age would also prevent extreme longevity from evolving, if "extreme" denotes a potential life span much longer than that imposed by extrinsic mortality in a given environment.) This and other arguments against the existence of an aging program have been discussed previously.

The evolutionary perspective sketched out above does not specify the mechanisms that underlie aging, but it helps to narrow down the possibilities. As already discussed, an evolved deterministic aging program can be ruled out, perhaps with the exception of specific niche situations. In the absence of adaptive life-curtailing processes driven by a putative aging program, we are left with untargeted pro-aging, destabilizing phenomena which, in principle, may range from purely stochastic to side-effects of "legitimate" biochemical pathways. These destabilizing forces are counteracted by evolved, and genetically controlled, longevity assurance (or repair/maintenance) processes. The interplay of these countervailing forces determines the life span.

While I have previously presented my detailed interpretation of this model, its central tenets bear repeating: (a) the destabilizing processes that drive aging are neither evolved nor adaptive; (b) in contrast, longevity assurance mechanisms are under genetic control; (c) together, these two opposing forces determine life span; (d) the average life span of a species is set by evolving longevity assurance mechanisms so as to optimize reproductive success under environmental conditions typical for that species.

Link: http://dx.doi.org/10.3389/fgene.2012.00189

Source:
http://www.fightaging.org/archives/2012/10/considering-longevity-in-terms-of-damage-versus-damage-repair.php

Stem cell therapies offer all sorts of possible ways to intervene in disorders of the brain and nervous system: the evidence suggests that, as for other parts of the body, there is a lot that can be achieved by dropping in a bunch of fully functional cells of the right type and letting them get to work. Or, alternately, by finding ways to stimulate existing cell populations into working harder.

Most of these approaches fall into the category of patches: increasing the pace of repair and recreation of destroyed resources, but doing little to address the underlying reasons for damage and destruction. As a strategy this is second-rate, especially in the brain, but it is how the mainstream of medical research proceeds. In part we can blame regulatory bodies for the focus on patching end results rather than preventing root causes: the way in which requirements and costs are imposed on the development of new therapies leads to a situation in which it the less expensive (and in some cases only) path is to build treatments for late stage disease.

Damage to myelin, the sheathing for axons in nerve cells, is at the root of a number of serious medical conditions. As is the case for most of our biology the integrity of myelin declines with age; some fraction of the age-related decline in cognitive function that occurs for everyone is thought to stem from progressively less effective myelination in the brain. A number of research groups are engaged in ongoing work with stem cells aimed at the repair of myelin, and here is one example:

Stem Cells Myelinate Human Brain

Neural stem cells transplanted into the brains of people with Pelizaeus-Merzbacher disease (PMD) can differentiate and begin producing the myelin sheaths that these patients lack, according to results of a Phase I clinical trial. ... If the stem cell transplants do ultimately demonstrate benefit, they could help more than just PMD patients ... There's a wide range of possible myelin disorders that could be targeted, including demyelinating disorders like multiple sclerosis and preterm babies at risk for cerebral palsy due to white matter injury.

Here, as in many other cases, a therapy is under development for use with specific named diseases - but it might also prove helpful as a treatment for aging, as an attempt to retard loss of cognitive function. Yet there is no path to legally produce therapies for general use in all old people in the US: the FDA doesn't recognize treatment of aging as a legitimate use of medicine, and short a revolution there's little hope of changing that situation through existing paths. Until this changes, a great deal of promising work will be sidetracked into narrow usage for late stage specific diseases, and any real progress towards clinical applications for aging will have to happen outside the US research community.

Source:
http://www.fightaging.org/archives/2012/10/stem-cell-transplants-as-a-way-to-regenerate-myelin.php

One line of research into treatments for neurodegenerative disorders involves spurring the brain to establish new neural connections to replace those that have been damaged or lost. This seems like an inferior strategy in comparison to trying to identify and remove root causes, one that can only delay the inevitable, but it's nonetheless a fairly entrenched field of work.

Here is an example of this sort of research - and note that as for other similar efforts there are hints that an induced increase in neural plasticity would be beneficial for cognitive function in all older individuals:

Researchers have developed a new drug candidate that dramatically improves the cognitive function of rats with Alzheimer's-like mental impairment. Their compound, which is intended to repair brain damage that has already occurred [by] rebuilding connections between nerve cells.

[The scientists] have been working on their compound since 1992, when they started looking at the impact of the peptide angiotensin IV on the hippocampus, a brain region involved in spatial learning and short-term memory. ... angiotensin IV, or early drug candidates based on it, were capable of reversing learning deficits seen in many models of dementia. The practical utility of these early drug candidates, however, was severely limited because they were very quickly broken down by the body and couldn't get across the blood-brain barrier.

Five years ago, [the scientists] designed a smaller version of the molecule [called] Dihexa. Not only is it stable but it can cross the blood-brain barrier. An added bonus is it can move from the gut into the blood, so it can be taken in pill form. The researchers tested the drug on several dozen rats treated with scopolamine, a chemical that interferes with a neurotransmitter critical to learning and memory. Typically, a rat treated with scopolamine will never learn the location of a submerged platform in a water tank, orienting with cues outside the tank. After receiving the [drug], however, all of the rats did, whether they received the drug directly in the brain, orally, or through an injection.

[The researchers] also reported similar but less dramatic results in a smaller group of old rats. In this study the old rats, which often have difficulty with the task, performed like young rats. While the results were statistically valid, additional studies with larger test groups will be necessary to fully confirm the finding.

Link: http://www.eurekalert.org/pub_releases/2012-10/wsu-pad101012.php

Source:
http://www.fightaging.org/archives/2012/10/treating-neurodegeneration-by-increasing-neural-plasticity.php