Jennifer Aniston At The Vanity Fair Party on Oscar Night

Called the quintessential California glamour girl, but a New Yorker at heart  Jennifer Aniston got a sun-kissed glow for the Academy Awards from makeup artist Angela Levin. Together Jennifer and Angela decided to create a look that screamed modern glamour. “Days before the Oscars she had returned from vacation and had a relaxed and glowing look, so it was perfect to go bronze and radiant” says Levin.

To get Jennifer’s look, Angela applied foundation using a brush over Jen’s already moisturized skin. Instead of a traditional blush, she dabbed a bit of Red creme lipstick on the apples of Aniston’s cheeks. A great back up when you don’t have a blush handy. And for extra radiance she used a shimmery bronze lotion and blended it onto the very top of her cheekbones and finished this gorgeous sun-kissed look with a dusting of loose bronzing powder.

I just loved her braid too. I know there were some fashionista’s were on the fence about her braided do, but I thought she looked great, and very fabulous at 40.

xx

image credit: Newscom

Image: Almay

Cosmetic companies are becoming fast aware of how many women are leaning towards products that are not only what they need, but also what the environment needs. Almay is the latest beauty company to get on the organic bandwagon, and just recently introduced their newest line of Eco-Friendly, Hypoallergenic, and natural products called Pure Blends. The newest generation of natural cosmetics for all those who are, have been, and plan to ‘Go-green’ when it comes to their beauty regime.

Ingredients like Lotus and Acai Extract, both anitoxidants that help protect the skin from free-radical damage, caused by over exposure to the sun and pollution are key ingredients in the product line. Also appealing is the pretty packaging that each product comes in which contains 44% recycled materials.

Everything you need from foundation, to blush, eyeshadows, and lip gloss. The eyeshadows last for hours and the colors are quite beautiful. My favorite lip gloss colors from the line are the Nude and Heather. They look great on and my lips feel so good.

The best thing about the entire line in addition to it being natural, is the price. Affordable and good, who can beat that:-)

xxoo

A couple of calorie restriction research papers caught my eye today, and I thought I’d share. First out of the gate is a study of one of a number of gene products associated with and necessary for the benefits of calorie restriction, but whose mechanisms are still poorly understood:

NQR1 controls lifespan by regulating the promotion of respiratory metabolism in yeast

The activity and expression of plasma membrane NADH coenzyme Q reductase is increased by calorie restriction (CR) in rodents. Although this effect is well established and is necessary for CR’s ability to delay aging, the mechanism is unknown.

Here we show that the Saccharomyces cerevisiae homolog, NQR1, resides at the plasma membrane and when overexpressed extends both replicative and chronological lifespan. We show that NQR1 extends replicative lifespan in a SIR2-dependent manner by shifting cells towards respiratory metabolism. Chronological lifespan extension, in contrast, occurs via a SIR2-independent decrease in ethanol production. We conclude that NQR1 is a key mediator of lifespan extension by CR through its effects on yeast metabolism.

The function of SIR2 in yeast is basically the same as SIRT1 in mammals, so it’s probably the case that we can learn about the function of plasma membrane NADH coenzyme Q reductase in mammals by looking at NQR1 in yeast. As things move forward in the investigation of metabolism and calorie restriction, I wouldn’t be surprised to see many different (possibly interacting) mechanisms that lead to essentially the same result, where cells are pushed towards greater levels of efficiency and recycling of damage.

But onwards to look at another study that provides confirmation of benefits resulting from the practice of calorie restriction.

The molecular architecture of myelinated peripheral nerves is supported by calorie restriction with aging

Peripheral nerves from aged animals exhibit features of degeneration, including marked fiber loss, morphological irregularities in myelinated axons and notable reduction in the expression of myelin proteins.

…

While calorie restriction (CR) is known to slow the aging process in the central nervous system, its influence on peripheral nerves has not been investigated in detail. To determine if dietary restriction is beneficial for peripheral nerve health and glial function, we studied sciatic nerves from rats of four distinct ages (8-, 18-, 29- and 38-months) kept on an ad libitum (AL) or a 40% CR diet.

Age-associated reduction in the expression of the major myelin proteins and widening of the nodes of Ranvier are attenuated by the dietary intervention

…

The improvements in nerve architecture with diet restriction, in part, are underlined by sustained expression of protein chaperones and markers of the autophagy-lysosomal pathway. Together, the in vitro and in vivo results suggest that there might be an age-limit by which dietary intervention needs to be initiated to elicit a beneficial response on peripheral nerve health.

The part about chaperones and autophagy refers to increased signs of cleanup of damaged cellular components taking place - which is thought to be one important way in which calorie restriction extends life. If you have less damage hanging around, on average, that damage will cause fewer additional problems. In this case it means nerves work better for longer.

Here’s a Russian press interview with biomedical gerontologist and radical life extension advocate Aubrey de Grey - which you might want to read through the Bable Fish translator:

[Interviewer] But - but as it is possible to interfere without the [full] understanding [of processes of aging]?

[Aubrey de Grey] We indeed interfere, without having precise knowledge about why cancerous tumor arose. Medicine generally frequently accomplishes the effective actions, not based on the precise knowledge. To take, for example, atherosclerosis, this “killer number is one” in the developed countries. We approximately visualize, as it is developed also it leads to what. But to mechanically destroy the cloth of atherosclerotic platelet we quietly can also without the knowledge about how this platelet it grows.

…

[Interviewer] But there are hundreds of fundamental scientists, connected with the problem experimentally. For example, they study the so-called “genes of aging”, but in this case they do not want to speak about the possibility to stop process itself. Why?

[Aubrey de Grey] The experiments of many scientists can prolong the life of cell, simplest organism, but I do not think that this will work at the level of man. However, the majority of researchers keep silent not therefore, but because they fear to lose financing. They depend on those average men themselves, who do not want to be charged by superfluous optimism, and therefore they are careful.

The quality isn’t great (it can translate “nematode” just fine, but produces artifacts like “it is still more important, here to eat the biologists”) but you’ll get the gist. The points quoted above are two of the most important considerations for advocacy:

• Firstly, that we can make significant progress in developing solutions to a problem in advance of complete understanding. I see the present debate over the level of effort to devote to development based on today’s knowledge to be the most important determinant of our future life spans. Will the research community get to work, or will it put off developing therapies for another few decades?
• Secondly that a strange self-perpetuating culture of conservatism and denigration about engineered longevity came into being in past decades, and must be shattered if we are to make progress.

An interesting opinion on the direction of aging research from a noted scientist in the field:

Virtually, all research on basic mechanisms of aging has used species that are short lived and thus demonstrably unsuccessful at combating basic aging processes. A novel comparative approach would use a diversity of populations and species, focusing on those with particularly long, healthy lives, seeking the causative mechanisms that distinguish them from shorter lived relatives.

Species of interest from this perspective include the naked mole rat, a mouse-size rodent that lives up to 30 years in the laboratory, and the little brown bat, which lives up to 34 years in the wild. Comparisons among dogs of different sizes, which differ by more than 50% in health span might also prove rewarding, as might novel species chosen because of their similarity to humans in certain key traits. Primates, because of their sophisticated cognitive ability, are a group of special value, and small, short-lived primates like the common marmoset might prove especially beneficial.

Cell repositories and tissue banks from key species, as well as genomic and analytic tools optimized for comparative studies, would make valuable contributions to a new comparative approach to basic aging research.

I see comparative studies - and the naked mole rat versus other rodents is a particularly good example - as a good way to reveal the relative importance of the various forms of cellular and molecular damage that cause aging. Is mitochondrial damage really so important in humans that it should be dealt with first of all, or are other types of damage just as limiting to life span, such that if mitochondria could be repaired, we wouldn’t gain much overall benefit? We don’t know for sure - though there’s nothing to be lost by moving ahead at full speed on all fronts of longevity science outlined in the Strategies for Engineered Negligible Senescence at this stage.