Halo Top is now vegan-friendly with these 7 flavors

Vegans and dairy-averse ice cream lovers: If you’ve been itching for, tweeting at, or sending carriers pigeons to Halo Top, hoping to secure just one dairy-free flavor, the company heard your pleas and happily complied. The cult-favorite, sort-of healthy ice cream purveyor just announced not one, but seven vegan-friendly flavors.

But what took them so long?!? According to Justin Woolverton, Halo Top founder and CEO, “It took a long time to ‘get it right,’ but we’re absolutely thrilled with the outcome.” Better late than never is always a true sentiment when it comes to creamy vegan treats.

Using coconut milk as a substitute, the brand re-created seven of its most in demand flavors.

Using coconut milk as a substitute, the brand re-created seven of its most in demand flavors—Peanut Butter Cup, Chocolate, Oatmeal Cookie, Sea Salt Caramel, Caramel Macchiato, Cinnamon Roll, and Chocolate Covered Banana. 

Halo Top’s popularity stems from its innovative flavoring (Mochi Green Tea, FTW) and healthier-than-most nutritional content (with 240 to 400 calories and around 20 grams of protein per pint). The new vegan offerings are no different, ranging from 280 to 360 calories and 12 grams of protein per pint, which is an added bonus when you’re living that meat-free lifestyle. But, as tempting as it may seem, beware of polishing off a pint in one sitting: Stevia helps keep Halo Top’s calorie counts low, but too much of the artificial sweetener might be a setback to your health goals.

A spokesperson from Halo Top said that while they can’t confirm the next vegan flavor offerings, “we can say that we are definitely excited to offer these vegan options to our fans, and although nothing is certain yet, we are looking forward to hopefully doing more in the future!”

The ice creams are available online now and will be in grocery stores by mid October, which is just in time for a Netflix-filled hygge season.

In the meantime, stock up on some dairy-free Haagen Dazs or make your own nice cream.

10 wellness experts on the most important relationship advice they’ve ever received

When seeking out counsel on how to avoid drama with your partner on vacation or establishing healthy relationship rules, it can be difficult to open up to the people around you (i.e. the ones who know your S.O.) about how his or her Monopoly win last night just totally wasn’t fair.

And if you need to have a talk about something like what’s happening in your sex life—or maybe even suggesting ways to spice things up—it can get awkward, fast.

But that’s where our Well+Good Council comes in. While no one ever figures it all out, this grounded group of health pros has some pretty genius dating and love advice, which they’re ready to pass along.

Read on for healthy relationship intel from wellness influencers like Candice Kumai, Kimberly Snyder, Norma Kamali, and more.

Continue reading 10 wellness experts on the most important relationship advice they’ve ever received

13 wellness experts on the gratitude practice that keeps them centered

Studies have shown that being optimistic and focusing on what makes you #blessed can banish stress—even just the simple act of acknowledging what you’re grateful for can have an impact on your overall happiness, studies show.

For some inspiration on how to develop a daily gratitude practice of your own, our Well+Good Council members are sharing their go-to ways to give thanks—heavy on the kindness and compassion.

Keep reading to learn more about how our handpicked health squad shows gratitude.
Continue reading 13 wellness experts on the gratitude practice that keeps them centered

FOXO Genes and Human Longevity

FOXO3A is one of the very few genes shown to have an association with human longevity in more than one study population, though this is neither a sizable nor reliable effect. We all age for the same underlying reasons, and on a schedule that should by rights be held as remarkable for its comparative lack of variation, rather than for the degree of variation we do observe. The scope of that natural variation in the processes of aging is a matter of thousands of individually tiny contributions from single genes, and most of that in the late stages of life, at the point where damaged systems are failing and flailing.

Those contributions are heavily dependent on one another, and vary enormously from individual to individual, from region to region, from lifestyle to lifestyle. That is why investigation of the genetics of long-lived individuals is not a field that will produce sizable gains in human longevity. It just isn’t the right place to find large improvements in human health, or ways to turn back aging rather than slightly reduce the pace at which it progresses. Nonetheless, considerably more effort has been put into this sort of genetic investigation than is put into approaches that are actually relevant to the development of actual, working rejuvenation therapies, as is illustrated by the overly enthusiastic paper on FOXO genes linked here.

Specific mechanisms involved in cellular processes that cause aging are a different story, however. FOXO4 has a role in maintaining the harmful state of cellular senescence, for example, and sabotaging that specific mechanism has been shown to selectively push senescent cells into self-destruction with little in the way of side-effects. All such senolytic therapies have the potential to produce sizable and reliable benefit. The point is that we shouldn’t be looking to natural variations between individuals as the place to find potential paths to treat aging. We should be looking to the causes of aging, and where they can be turned back most effectively.

Several pathologies such as neurodegeneration and cancer are associated with aging, which is affected by many genetic and environmental factors. Healthy aging conceives human longevity, possibly due to carrying the defensive genes. For instance, FOXO (forkhead box O) genes determine human longevity. FOXO transcription factors are involved in the regulation of longevity phenomenon via insulin and insulin-like growth factor signaling. Only one FOXO gene (FOXO DAF-16) exists in invertebrates, while four FOXO genes, that is, FOXO1, FOXO3, FOXO4, and FOXO6 are found in mammals. These four transcription factors are involved in multiple cellular pathways, which regulate growth, stress resistance, metabolism, cellular differentiation, and apoptosis in mammals.

FOXOs are mainly involved in the regulation of metabolism, regulation of reactive species, and regulation of cell cycle arrest and apoptosis. FOXO1 regulates adipogenesis, gluconeogenesis, and glycogenolysis. Mechanistically, the unphosphorylated FOXO1 binds to the insulin response sequence present in the promoter region of G6P (glucose-6 phosphatase) in the nucleus. It leads to the accelerated transcription resulting in the enhanced production of glucose in the liver. Adipogenesis is negatively regulated by FOXO1 through its binding to the promoter region of PPARG (peroxisome proliferator-activated receptor gamma) and inhibiting its transcription. Moreover, FOXO1 functions as an association between transcription and insulin-mediated metabolic control; thus, FOXO1 is a promising genetic target to manage type 2 diabetes.

FOXO3 probably induces apoptosis either upregulating the genes needed for cell death or downregulating the anti-apoptotic factors. In addition, FOXO3 has been found to regulate the Notch signaling pathway during the regeneration of muscle stem cells. Moreover, antioxidants are thought to be upregulated by FOXO3 to protect human health from oxidative stress. Additionally, FOXO3 is documented to suppress tumour growth. Thus, tumour development may occur if FOXO3 is deregulated. Most importantly, FOXO3 are described to play a role in long-term living.

FOXO4 is involved in the regulation of various pathways associated to apoptosis, longevity, cell cycle, oxidative stress, and insulin signaling. FOXO4 is associated with longevity through the insulin and insulin-like growth factor signaling pathway. Finally, mutation-triggered Akt phosphorylation results in the inactivated FOXO4. It deregulates the cell cycle and activates kinase inhibitors involved in the cell cycle. It leads to the prevention of tumour progress into the G1 phase of cell division.

Numerous strategies for future research can be predicted. For instance, the triggering of FOXO-mediated processes in the tissues with metabolically different features can be valuable to explore the mechanism of FOXO-mediated longevity. In addition, the human FOXO sequence variations and their effect on the resulting proteins should be studied, the possible findings can also reveal the underlying mechanisms of FOXO-induced healthy aging. The delay in age-related pathologies including cancer and neurodegenerative diseases and living long life depends on the control of morbidity. It is therefore an exciting area of study to investigate potential antiaging compounds; however, their testing in clinical setup would need biomarkers to assess aging rate. Owing to the potential effect of FOXOs on health issues, the future therapies could be based on the FOXOs.

Link: http://bit.ly/2fxVSFC

📍

Lipid Peroxidation and APOE Variants in Alzheimer’s Disease

Researchers here report on the role of lipid peroxidation in the pathology of Alzheimer’s disease, in particular as a way to explain why some variants of apolipoprotein E (APOE) appear to be linked to a greater risk of developing this neurodegenerative condition. Alzheimer’s is a complex biological failure state built of many interdependent chains of cause and effect, and thus the one small area touched on in this research, somewhere in the midst of this sea, can be linked to a range of other processes and failures observed in the brain tissue of patients and animal models. To pick a few examples: rising levels of inflammation and oxidative stress; the failure of lysosomes – and thus failure to recycle metabolic waste – in the glial support cells in the brain; and also the changing behavior and generally greater dysfunction of these glial cells with increasing age.

Researchers discovered in 2015 that a number of genes involved in neurodegeneration promote damage to neurons and glia by inducing high levels of free radicals (oxidative stress) and accumulation of lipid droplets in glia. This work sets the stage for the current study. “Using electron microscopy, we observed lipid droplet accumulation in glia before obvious symptoms of neurodegeneration. In the presence of high levels of oxidative stress, neurons produce an overabundance of lipids. The combination of free radicals and lipids, which produces peroxidated lipids, is detrimental to cellular health. Neurons try to avoid this damage by secreting these lipids, and apolipoproteins – proteins that transport lipids – carry them to glia cells. Glia store the lipids in lipid droplets, sequestering them from the environment and providing a protective mechanism.”

The team discovered that the storage of lipid droplets in glia protects neurons from damage as long as the free radicals do not destroy the lipid droplets. When the lipid droplets are destroyed, cell damage and neurodegeneration ensues. “Our research brought us to a fascinating and unexpected finding. Approximately 15 percent of the human population carries apolipoprotein APOE4. Since APOE4 was first linked to Alzheimer’s disease almost 30 years ago, it remains the strongest known genetic risk factor for this disease. Meanwhile, APOE2, which is slightly different from APOE4, is protective against the disease. This evidence suggests that APOE is important for proper brain function, but we know little about how APOE itself may lead to Alzheimer’s disease”.

The researchers found that apolipoproteins APOE2, APOE3 and APOE4 have different abilities to transfer lipids from neurons to glia and hence differ in their ability to mediate the accumulation of lipid droplets. “APOE2 and APOE3 can effectively transfer lipids into glia. On the other hand, APOE4 is practically unable to carry out this process. This results in a lack of lipid droplet accumulation in glia and breakdown of the protective mechanism that sequesters peroxidated lipids. This fundamental difference in the function in APOE4 likely primes an individual to be more susceptible to the damaging effects of oxidative stress, which becomes elevated with age.”

Link: http://bit.ly/2wnzF3O

📍

How to use your garden tomatoes to make an upgraded Bloody Maria

Laura Silverman
The Outside Institute founder Laura Silverman; Photo: Mark Hanauer

Whether you buy your tomatoes at the farmers’ market or grow your own right in the backyard, these last few weeks of warm weather are ideal for making the most of your bounty. But before you use them all in a homemade sauce for your caulicrust pizza or a caprese salad, you’ll definitely want to set aside a vine’s worth for this boozy weekend favorite: an upgraded Bloody Maria, courtesy of Well+Good’s resident cocktail expert, The Outside Institute founder, Laura Silverman.

“The bumper crop of late-season tomatoes makes summer last just a little bit longer,” she says. “I use it to make tomato water—infused with the intense flavor of the fruit and herbs—to make a cold drink that’s made even better with just a little tequila.”

Health bonus: Tomatoes are ripe with carotenoids—including lycopene—which means they’re loaded with antioxidants. Silverman keeps her recipe sugar free, instead adding a subtle sweetness to the cocktail with blue agave nectar. And instead of celery, she uses cilantro to add the perfect finishing touch.

Ready to make this upgraded Bloody Maria? Keep reading for the recipe.

Continue reading How to use your garden tomatoes to make an upgraded Bloody Maria

How to tell if you actually have candida overgrowth (and what that actually means)

These days, you may consider yourself a champion kombucha swigger (and probiotic popper, for that matter), but there’s still one gut-health topic you might not be talking about: Candida.

And it might be time to actually have that conversation. “When people hear the term Candida, they automatically think of a bogeyman,” says Mahmoud A. Ghannoum, PhD, who’s been studying Candida for more than 40 years. “But it’s actually quite normal to have it in the gut.”

So, what exactly is it? Candida is a fungus (or form of yeast) that’s part of the microbes that live in your gastrointestinal tract—and that’s not necessarily a bad thing. “It’s very common in 70 percent of the population,” says Dr. Ghannoum, who should know—he’s the scientist who named the mycobiome, or community of fungi living in your gut. “So even when you have a normal healthy gut, it’s more than likely you’ll have Candida in there.”

But Candida overgrowth is when things can get tricky. This overgrowth can lead to infection, which can cause a myriad of health problems including digestive issues, yeast infections, and chronic fatigue. And sometimes it’s difficult to figure out when this is going on.

To solve this, Dr. Ghannoum created the BIOHM Candida Report, an at-home kit that helps you keep tabs on the Candida levels in your gut’s microbiome. “If left unchecked, Candida overgrowth can have a tremendous impact on your health and wellness in a wide variety of ways,” he warns.

The kit includes everything you need to take a small fecal sample (nobody said gut health was glamorous) which you’ll then send off to the BIOHM labs. Once it’s analyzed, you’ll get a report telling you the different types of Candida species present in your gut, as well as the specific levels of each one.

If you actually have Candida overgrowth, it’s important to figure out the proper next steps. According to Dr. Ghannoum, that could be as simple as upgrading your diet and changing your probiotic and prebiotic regimen. “And if you’re dealing with substantial Candida overgrowth, your physician would likely prescribe an antifungal medication,” he adds.

Scroll down to learn how you can determine if you have Candida overgrowth—and why it’s important to find out.

Continue reading How to tell if you actually have candida overgrowth (and what that actually means)

Suppressing Wnt/β-catenin Signaling to Reduce Cardiac Fibrosis after Injury

Fibrosis is the result of dysfunctional regenerative processes, such as those operating in old tissues. Instead of rebuilding the structures that should exist, instead regeneration is characterized by the formation of scar-like collagen deposits that disrupt normal tissue layout and function. This is particularly important in the age-related decline of organs such as the kidney, lung, liver, and heart: where correct function is absolutely vital, or where precise tissue structure is absolutely vital. Regeneration is a coordinated dance between immune cells, senescent cells, and the cells that will do the work of rebuilding: a mix of stem cells, progenitor cells of various types, and ordinary somatic cells. With age, the immune system becomes inflammatory and disarrayed, stem and progenitor cells are less activity, and growing numbers of persistent senescent cells pump out signals that disrupt the intricate relationships needed for regenerative processes to operate.

Recent research is making it clear that lingering, persistent senescent cells are an important cause of fibrosis. However, it remains the case that most researchers interested in fibrosis are still operating in the paradigm of mapping regulatory genes and proteins throughout a tissue, rather than looking for a set of cells that are at fault. The mapping proceeds in the hope of finding target proteins that can be blocked, enhanced, or otherwise manipulated in order to change cell behavior during regeneration – to dial down fibrosis. In the paper noted here, the authors settle on Wnt/β-catenin signaling as a potential target, and indeed demonstrate that absent this signaling process mice produce less scarring and fibrosis after injury to heart tissue.

If you read through the paper, there isn’t any mention given to cellular senescence, but we can look elsewhere to find a number of studies that implicate Wnt/β-catenin signaling in the machinery and reactions that push cells into a senescent state. So what these researchers appear to have demonstrated is that reducing the degree to which heart injury results in increased cellular senescence also reduces fibrosis and scarring – which dovetails nicely with what other researchers are uncovering of the role of senescent cells in this aspect of aging. Suppressing the creation of senescent cells isn’t, to my eyes, as desirable as destroying them after the fact with senolytic therapies, however. Senescent cells do have a transient role to play in healing. Continual suppression will make healing less effective overall, even as it reduces fibrosis in older individuals. On the other hand, periodic elimination of lingering senescent cells should allow patients to obtain all of the benefits of reduced inflammation, unimpaired regeneration, and minimal fibrosis.

Study Explores the Biology of Mending a Broken Heart

The Wnt/β-catenin signaling pathway is involved in several of the body’s fundamental biological processes. After heart injury, however, Wnt/β-catenin signaling ramps up in cardiac fibroblast cells to cause fibrosis, scarring and harmful enlargement of the heart muscle, according to the researchers. “Our findings provide new insights on what causes cardiac fibrosis and they open the potential for finding new therapeutic approaches to fight it and preserve heart function. Wnt/β-catenin signaling is involved in many normal and disease processes and it’s tough to target therapeutically. But the idea that early targeting of fibrotic response in cardiac disease may improve muscle function and stop disease is an exciting new direction.”

In the current study, researchers used a newly developed line of genetically bred laboratory mice that allowed them to determine how important Wnt/β-catenin signaling is in cardiac fibroblast cells. Fibroblasts are important to building the connective tissues and structural framework cells that help hold the body together. But in the context of heart disease, researchers are learning resident cardiac fibroblast cells cause a deadly mix of tissue fibrosis, scarring and diminished function.

To simulate cardiac injury in the mice, researchers conducted a procedure called trans-aortic constriction to restrict blood flow through the heart. Some of the mice were bred so that following cardiac injury they did not express cardiac Wnt/β-catenin in fibroblasts. Control mice in the study continued to express Wnt/β-catenin following heart injury. The control mice exhibited extensive fibrosis, scarring, and diminished heart function. Mice not expressing Wnt/β-catenin had diminished fibrosis and scarring and the animals’ heart function was preserved.

Loss of β-catenin in resident cardiac fibroblasts attenuates fibrosis induced by pressure overload in mice

Cardiac fibrosis, commonly seen with a variety of cardiac injuries, can significantly reduce tissue compliance and disrupt cardiac conduction, thus contributing to morbidity and mortality associated with heart disease. The hallmark of cardiac fibrosis is increased fibrillar collagen, which contributes to reduced cardiac output and can ultimately lead to heart failure. Cardiac fibroblasts (CFs) that arise from epicardial and endothelial progenitors in the developing heart are the predominant collagen-producing cell type in pathologic cardiac fibrosis. Although these resident CFs maintain a quiescent phenotype under physiological conditions, they can be activated in response to various types of cardiac injury. Importantly, the regulatory mechanisms that lead to increased collagen production from resident CFs under pathophysiologic conditions, ultimately leading to heart failure, have not been fully elucidated.

Wnt/β-catenin signaling is induced in areas of inflammation, scar formation, and epicardial activation in mouse models of ischemic injury. However the role of Wnt/β-catenin signaling in myocardial interstitial fibrosis independent from scar formation has not been determined. In addition, the requirement for Wnt/β-catenin signaling specifically in resident CFs and direct downstream targets related to cardiac fibrosis have not been reported previously. Recently developed inducible Cre-expressing mouse lines are effective for manipulation of gene expression in resident CF lineages. Using this approach to specifically target activated CFs is of use in studies of CF-specific regulatory mechanisms in cardiac fibrosis.

The requirements for Wnt/β-catenin signaling specifically in resident and activated CFs after cardiac pressure overload were examined using an engineered loss of β-catenin. Here, we demonstrate that cardiac pressure overload leads to increased Wnt/β-catenin signaling in CFs, while loss of β-catenin results in improved cardiac function, blunted cardiac hypertrophy, reduced interstitial fibrosis and decreased expression of fibrotic extracellular matrix (ECM) protein genes 8 weeks post trans-aortic constriction (TAC). Further, β-catenin loss of function mutation in CFs directly reduces cardiomyocyte hypertrophy. Together, these data support a regulatory role for Wnt/β-catenin signaling in fibrosis due to CFs after cardiac injury.

📍