“Whole fruit is nothing but good for people who have prediabetes,” Wright says. Just don't consume produce in the form of juice or smoothies. “Though a smoothie does give one a concentrated source of nutrients, they are often packed with calories that don’t satisfy our hunger as there is little fiber in them,” Denison says. So rather than drinking your fruit, eat it, spacing it out over your day.
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In Alzheimer’s disease (AD), the function of the brain is compromised by the buildup of debris (plaques and tangles) inside the neurons. This mainly occurs in the areas of the brain associated with memory, intelligence, judgement, behaviour and language and impairs the ability to complete normal day to day tasks and to interact socially. Whilst the symptoms of AD usually only begin to appear with age, evidence suggests that damage to the brain begins to accumulate years earlier. This includes the buildup of plaques and tangles and a decreased ability to metabolise glucose (brain insulin insensitivity)50. If an individual has Type 2 Diabetes (systemic insulin insensitivity), the risk of AD is tenfold higher51.
309. Lemieux K., Konrad D., Klip A., Marette A. The AMP-activated protein kinase activator AICAR does not induce GLUT4 translocation to transverse tubules but stimulates glucose uptake and p38 mitogen-activated protein kinases alpha and beta in skeletal muscle. FASEB Journal. 2003;17(12):1658–1665. doi: 10.1096/fj.02-1125com. [PubMed] [CrossRef] [Google Scholar]
Blood pressure goals are generally set lower than 130/80. Some blood pressure medications offer more benefits than simply lowering blood pressure. For example, a class of blood pressure drugs called ACE inhibitors has been found to also reduce the levels of insulin resistance and actually deter the development of type 2 diabetes. This is an important consideration when discussing the choice blood pressure drugs in the metabolic syndrome.
^ Jump up to: a b Cardona A, Pagani L, Antao T, Lawson DJ, Eichstaedt CA, Yngvadottir B, Shwe MT, Wee J, Romero IG, Raj S, Metspalu M, Villems R, Willerslev E, Tyler-Smith C, Malyarchuk BA, Derenko MV, Kivisild T (2014). "Genome-wide analysis of cold adaptation in indigenous Siberian populations". PLOS One. 9 (5): e98076. Bibcode:2014PLoSO...998076C. doi:10.1371/journal.pone.0098076. PMC 4029955. PMID 24847810.

sdLDL. This is a measurement of the number of small dense low-density lipoprotein molecules a person has. LDL varies in size, and the smaller denser molecules, which tend to form when elevated triglycerides and VLDL are present in the blood, are thought to be more aggressive in causing atherosclerosis. This test is now commercially available, but is not performed by many laboratories and is not ordered frequently. Its ultimate clinical utility has yet to be determined. It may be evaluated in a LDL particle testing.
Concussion (a mild form of TBI), is defined as a short term impairment of brain function caused by impact. Symptoms include dizziness, confusion and headache. When the brain suffers a concussive impact this triggers an acute cascade of cellular events that can eventually cause chronic problems. Firstly, immediately after impact there are changes to the concentrations of ions and neurotransmitters in and outside of the neurones. For example, the cells release potassium and glutamate (excitatory neurotransmitter); this can cause neuronal damage instantly64. The disruption to the equilibrium of substances within the brain must be corrected, which requires the action of the ATP dependant ion pumps in the cell membranes. In order to produce enough ATP the brain has a transient period of high glucose metabolism (within 30 minutes of impact), which is followed by a period of glucose metabolic depression that can last anywhere from 5 days to several months, depending on severity65. In this time the brain is starved of energy when it is unable to metabolise glucose, which can cause long term damage. Severe or repeated impacts can lead to development of conditions such as chronic traumatic encephalopathy (CTE). 
Although mitohormesis has not been studied comprehensively in higher-level organisms, its occurrence is supported by compelling evidence in lower-level organisms. For example, inhibition of glycolysis in C. elegans increased fat oxidation (based on nematode triglyceride content) and mitochondrial O2 consumption, which was followed by increases in ROS production at day 2 and catalase activity at day 6 [72]. The increase in catalase activity occurred in conjunction with increases in lifespan and resistance to the mitochondrial stressors sodium azide and paraquat. However, antioxidant treatment (N-acetylcysteine) decreased the elevation of ROS at day 2 and eliminated the resistance to sodium azide and paraquat treatments, indicating a requirement of ROS as a stimulus [72].
I contracted hsv from my ex partner we broke up the relationship about four years ago, I has been on treatment for some years, I had lot pains and embarrassment for been Hsv patient last two month i did Hsv research online and found website for natural treatment to get ride of my infection, and i went through the site and recommend me to Dr Ben I contacted Dr Ben through his website and been his patient after one month I got cured. I want everyone living with Hsv to get this treatment and got cured Dr Ben have the cure to every virus. his email;
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Nutritional ketosis may facilitate PGC-1α activity through multiple mechanisms. Since PGC-1α is activated by AMPK and SIRT1, nutritional ketosis may initiate PGC-1α activity through these enzymes. As previously mentioned, catecholamines and adiponectin facilitate PGC-1α activity by promoting its expression, and insulin inhibits PGC-1α through downstream phosphorylation, all independent of AMPK. As previously discussed, a ketogenic diet may increase catecholamines and adiponectin and is well known to decrease insulin, indicating that nutritional ketosis may directly facilitate PGC-1α activity through these hormones. Supporting these potential mechanisms, a ketogenic or low-carbohydrate diet has increased expression, protein content, and activation of PGC-1α [149, 231, 317], as well as expression of its target PPARα [87, 148]. Furthermore, in skeletal muscle of mice following a ketogenic diet, the resulting increases in O2 consumption and expression of genes related to fat oxidation appear to be dependent on PGC-1α [157]. Ketones likely contribute to this signaling as well based on the recent observation that the increased hepatic expression of PPARα targets induced by a ketogenic diet did not occur with a nonketogenic low-carbohydrate diet [37].
PGC-1α coactivates all three known PPAR isoforms (PPARα, PPARδ, and PPARγ) [286]. Although each isoform is expressed in a variety of tissues, PPARα is prominently expressed in the liver, PPARδ in skeletal muscle, the heart, and the pancreas, and PPARγ in adipose [286, 296]. PGC-1α was discovered and named based on its promotion of brown adipose differentiation through coactivation of PPARγ and subsequent induction of mitochondrial biogenesis and UCP1 expression [297]. However, it is the PGC-1α coactivation of PPARα that is responsible for the upregulated transcription of many of the enzymes responsible for increased ketogenesis and fatty acid metabolism in response to a ketogenic diet [120]. Consistent with the role of PGC-1α in inducing mitochondrial biogenesis, it also shifts skeletal muscle fiber composition towards type I [298, 299] and type IIa [299], which are more oxidative. AMPK also contributes to fiber type changes and is required for the transition of highly glycolytic, type IIb fibers to more oxidative, type IIa fibers [276]. Although PGC-1α is primarily known for inducing transcription of nuclear DNA, it may also, in conjunction with SIRT1, induce expression of mtDNA [300].

It is still unclear what is the very first step that occurs in a normal cell becoming cancerous. Two theories that explain the development of cancer are the ‘somatic mutation’ theory, and the ‘metabolic theory.’ The somatic mutation theory states that the first event in cancer is a gene mutation due to environmental damage or a mistake in the DNA replication and repair processes. This gene mutation initiates a cascade of events that subsequently leads to tumour growth. Popular opinion favoured the somatic mutation theory for many years, leading to a large body of research describing the different genetic mutations of cancer cells, and ambitious projects to sequence the ‘Cancer Genome.’ From the compelling simplicity of the somatic mutation theory, an increasingly complicated picture has emerged as more than 100 oncogenes and 30 tumor suppressor genes have been identified, leading researchers to look for alternative explanations. 
As ketones are the only other metabolic substrate that can fuel the brain, there is a compelling mechanism whereby ketosis could improve brain energy metabolism and therefore improve symptoms of AD. Despite a declining ability of the brain to use glucose, cerebral ketone metabolism is preserved in AD (Castellano2015). This means that ketosis could be used to prevent an energy deficit in the brain. Another possibility is that ketone metabolism decreases mitochondrial damage caused by oxidative stress in the brain52. Individuals with AD tend to have increased mitochondrial oxidative stress, which can worsen brain energy production and increase plaque and tangle formation53.  

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In 2005, the American Heart Association (AHA) in conjunction with the NHLBI also released a scientific statement regarding metabolic syndrome that includes a set of criteria that defines the condition. In order to provide more consistency in both patient care and research, the International Diabetes Federation, NHLBI, AHA, World Heart Federation, and the International Association for the Study of Obesity published a joint statement in 2009 that describes a "harmonized" definition of metabolic syndrome. Waist circumference, with population and country-specific criteria, replaced obesity as a measure of body status.
Thanks for this inputs. 20 years ago I gain 17 pounds a year for 5 years. I was healthy but my dr told me start diet, any diet just come back in a month I want to see you start loosing… I started Atkins and lost 7 pound in a month. She was checking my progress every six months and checking my condition. I lost 64 pounds in 3 years. Now I started eating out of control. I am eating healthy but too much… I gain 40 pound back after 20 years. Now I will start again my Atkins to take off 30 pounds…
Jennifer, The yeast has no carbs. The coconut sugar does have carbs, but the yeast feeds on it and through the process of fermentation uses the sugar for energy and releases carbon dioxide gas as a result. The yeast is for flavor, aroma, and in our opinion does help with a little bit of rise. Additionally, we don’t like to consider any foods “bad”, “off-limits”, or not keto. Instead, we opt to mainly eat nourishing real foods that fit into our daily macro intake. We hope this helps! Best of luck on your keto journey.
Did you hear the news? I have a new cookbook out called Keto Instant Pot Recipes book! But this is not just any Instant Pot cookbook. This keto cookbook has a ton recipes with BOTH Instant Pot directions AND slow cooker directions! I also started an Instagram account on my favorite Keto Instant Pot Recipes and giveaways called @KetoInstantPotRecipes! 
Keto Bread Recipe - Four Ways - quick and simple way to make low carb, individual keto bread rolls, in ramekins and just a few healthy ingredients. You can either bake it in the microwave for 90 seconds or in the oven for 10-15 minutes. The the-easiest, the-best kept bread recipe I've ever tried. There are four different options available - you can make cheese keto bread,  broccoli ketogenic bread, bacon and spinach and feta. And of course you can leave it as it is, if you prefer plain kept bread  rolls.
Though the hunger-reduction phenomenon reported during ketogenic diets is well-known, the underlying molecular and cellular mechanisms remain uncertain. Ketosis has been demonstrated to exert an anorexigenic effect via cholecystokinin (CCK) release while reducing orexigenic signals e.g., via ghrelin. However, ketone bodies (KB) seem to be able to increase food intake through AMP-activated protein kinase (AMPK) phosphorylation, gamma-aminobutyric acid (GABA) and the release and production of adiponectin. The aim of this review is to provide a summary of our current knowledge of the effects of ketogenic diet (KD) on food control in an effort to unify the apparently contradictory data into a coherent picture.
What causes high cholesterol? High cholesterol is a risk factor for heart attacks and coronary heart disease, because it builds up in the arteries, narrowing them. It does not usually have any symptoms, and many people do not know they have it. We look at healthy levels and ranges of cholesterol, at ways to prevent it, and medications to treat it. Read now
Formation of O2•− at complexes I and III primarily occurs in the mitochondrial matrix, but some of the O2•− produced at complex III is produced in the intermembrane space [63]. Within the matrix, O2•− is rapidly dismutated into hydrogen peroxide (H2O2) by manganese superoxide dismutase (SOD2) [41, 53]. Some O2•− may escape into the mitochondrial intermembrane space [64] and cytosol [65], where copper/zinc superoxide dismutase (SOD1) can dismutate it into H2O2 [41]. The large majority of mitochondrial H2O2 is removed by peroxiredoxin (Prx) 3, followed by much smaller contributions from Prx5 and glutathione peroxidases (GPx) 1 and 4 [66]. GPx also removes other peroxides, including lipid hydroperoxides [41]. Catalase is another antioxidant enzyme capable of removing H2O2 but is primarily located in peroxisomes and is therefore unlikely to directly remove mitochondrial H2O2 [41, 66]. However, H2O2 can be transported out of mitochondria [67], and it is possible that the majority of mitochondrial H2O2 is removed in the cytosol. Since Prxs and GPxs rely on NADPH for recycling of their cofactors (thioredoxins and glutathione, resp.) [41], and since NADH is required for recycling of NADPH [68], activity of these enzymes would decrease availability of NADH for oxidative phosphorylation. Therefore, transport of H2O2 out of mitochondria for removal in the cytosol may be a more likely defense mechanism [67], implying a more important role of catalase and other antioxidant enzymes outside of mitochondria. Despite the lower reactivity of H2O2, it is still reactive and can oxidize metal ions, particularly iron, to form the hydroxyl radical (•OH), which readily damages DNA, lipids, and proteins [41]. •OH is scavenged by metallothioneins I and II [69, 70] and glutatathione [71], indicating that these antioxidant proteins may be important defenses against byproducts of unaddressed mtROS. Other important antioxidant enzymes include glutamate-cysteine ligase (GCL), which is the rate-limiting step in glutathione synthesis, and glutathione reductase (GSR) and thioredoxin reductase (TRXR), which recycle glutathione and thioredoxin, respectively, to their reduced forms [41].
The ketogenic diet is high-fat and low-carb, and if you pay attention to food and nutrition trends, then you already know that creative recipes for this weight-loss plan are all over social media. If you've gone keto or are thinking of trying it, check out these tasty morning meal ideas to help you stay full, score energy, and leave you feeling satisfied.

I’m discouraged to see that nowhere in the article nor in the comments is there a mention of a diet’s best fit to genetics. Consider if someone is an APOE E2 carrier and/or has certain polymorphisms of the APO5 gene. These are quite rare in Okinawa but much more prevalent in the USA (12% of the population). According to a number of well-designed studies, these genetic characteristics point to a higher fat, lower carbohydrate diet as beneficial and even a “moderate” carb diet as problematic.


Although the first formal definition of metabolic syndrome entered medical textbooks not so long ago (1998), it is as widespread as pimples and the common cold . According to the American Heart Association, 47 million Americans have it. That's almost a staggering one out of every six people. The syndrome runs in families and is more common among African-Americans, Hispanics, Asians, and Native Americans. The risks of developing metabolic syndrome increases as you age.
The last issue is your consumption of “residual” carbohydrates—the carbs you’re not even aware you’re eating, like those in nuts and meal-replacement shakes. It’s OK to have some nuts, but you should rely more on other fat sources that are carb-free like oils and cheeses. Remember that meal replacement shakes and protein shakes are not the same. The typical meal-replacement powder contains up to half your day’s intake of carbs. Instead, opt for a scoop of regular protein powder after your workout. Make these changes and you’ll see your six-pack soon enough.
Hi Maria- I am a 3 year cancer survivor. I had been following basically a paleo diet, but often fell off the wagon where sugar was concerned. In the last year I was diagnosed with ulcerative colitis and chrohn’s disease. My naturopath recommended I follow the keto-adaptive diet. I was very excited to make your amazing bread, but I wonder if the psyllium powder would be bad for my intestinal issues? Hope not!
Hi there, how many slices you get really depends on the kind of loaf pan you use. I find I get around 20 slices for a bread made in the regular loaf pan (though with this recipe they will be rectangular rather than square) and 12-14 slices using a small loaf pan as described in the post. That’s why I decided to state a portion size – 12 per bread. 1 portion = 0.6 net carbs

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Metabolic syndrome is quite common. Approximately 32% of the population in the U.S. has metabolic syndrome, and about 85% of those with type 2 diabetes have metabolic syndrome. Around 25% of adults in Europe and Latin America are estimated to have the condition, and rates are rising in developing East Asian countries. Within the US, Mexican Americans have the highest prevalence of metabolic syndrome. The prevalence of metabolic syndrome increases with age, and about 40% of people over 60 are affected.
Hi Brenda, There are various reasons but the most common one is that coconut flour is extremely absorbent and needs a lot of eggs to offset how much moisture it absorbs. If you used a liquid like milk or water, it would fall apart. That being said, this recipe is not dry or dense. Did you try making it? Whipping the egg whites creates the exact opposite effect and the bread turns out light and fluffy. Hope you’ll give it a try!
Some Inuit consume as much as 15–20% of their calories from carbohydrates, largely from the glycogen found in raw meats.[43][44][47][45][50] Furthermore, the blubber, organs, muscle and skin of the diving marine mammals that the Inuit eat have significant glycogen stores that are able to delay postmortem degradation, particularly in cold weather.[51][52][53][54][55][56]
Embarrassing admission: I remember exactly where I was sitting in a clinic at Johns Hopkins in 2002 explaining to (admonishing, really) a patient who was on the Atkins diet how harmful it was because of DKA.  I am so embarrassed by my complete stupidity and utter failure to pick up a single scientific article to fact check this dogma I was spewing to this poor patient. If you’re reading this, sir, please forgive me. You deserved a smarter doctor.
One particular concern to be aware of is the risk for ketoacidosis, which especially applies to diabetics. Ketoacidosis is a dangerous metabolic state in which excessive amounts of ketones are produced. In mostly healthy individuals, ketosis is regulated by insulin, which is the hormone that controls the creation of ketone bodies and regulates the flow of fatty acids into the blood.
Ketones are a special type of fat that can stimulate the pathways that enhance the growth of new neural networks in the brain. A ketogenic diet is one that is high in fats, and this diet has been a tool of researchers for years, used notably in a 2005 study on Parkinson’s patients finding an improvement in symptoms after just 28 days. The improvements were on par with those made possible via medication and brain surgery. Other research has shown the ketogenic diet to be remarkably effective in treating some forms of epilepsy, and even brain tumors.
While it is believed that carbohydrate intake after exercise is the most effective way of replacing depleted glycogen stores,[72][73] studies have shown that, after a period of 2–4 weeks of adaptation, physical endurance (as opposed to physical intensity) is unaffected by ketosis, as long as the diet contains high amounts of fat, relative to carbohydrates.[74] Some clinicians refer to this period of keto-adaptation as the "Schwatka imperative" after Frederick Schwatka, the explorer who first identified the transition period from glucose-adaptation to keto-adaptation.[75]
Attempt #4 or 5, I lost count 🙂 I measured everything by weight (ounces and grams as you listed) not by cups or tsps, etc. Put in oven at 375 since I don’t have convection and the previous attempts didn’t rise. This one rose beautifully! Nice beautiful color! Cooked 80 minutes. Let cool completely in my 8×4 metal loaf pan. Several hours later, I decided to take out of pan and cut a slice. It caved a little in on the sides, it looks similar to your 12 oz water picture, but it is wet. I’m not sure you’d call it gummy but definitely too much moisture again. And, I thought I finally had one! Back to the testing…I’ve gone thru 1/2 my Honeyville 5 lb bag and haven’t had one successful loaf yet 🙁

After a period of time, your body becomes adapted to using ketones as fuel instead of glucose. Your muscles begin to learn to convert acetoacetate into a ketogenic substance called beta-hydroxybutyrate, or BHB. BHB then becomes the new preferred ketogenic source of energy, including to fuel all brain activity. What is not needed is expelled from the body as waste.
We can say that no species, including humans, could have survived for millions of years without the ability to withstand brief periods of hunger or starvation (Amen-Ra, 2006). These periods of fasting are themselves ketogenic (McCue, 2010) during which the concentrations of insulin and glucose decrease while that of glucagon increases in the attempt to maintain normal blood glucose levels. When the body passes from a condition of food abundance to one of deprivation (or else via VLCKD simulated deprivation), there is, with a slight delay, an increase in the concentration of free FAs as well as KB in the blood. Thus, from this point of view KD could be compared to caloric restriction for fasting. These manipulations of nutrients, both in quantity and quality, seem to not only act on blood glucose/KB level but also to promote changes in metabolic pathways and cellular signaling. How this kind of metabolic condition (ketosis) can affect satiety and hunger mechanisms is still a matter of debate.
Dietary fiber intake provides many health benefits. However, average fiber intakes for US children and adults are less than half of the recommended levels. Individuals with high intakes of dietary fiber appear to be at significantly lower risk for developing coronary heart disease, stroke, hypertension, diabetes, obesity, and certain gastrointestinal diseases. Increasing fiber intake lowers blood pressure and serum cholesterol levels. Increased intake of soluble fiber improves glycemia and insulin sensitivity in non-diabetic and diabetic individuals. Fiber supplementation in obese individuals significantly enhances weight loss. Increased fiber intake benefits a number of gastrointestinal disorders including the following: gastroesophageal reflux disease, duodenal ulcer, diverticulitis, constipation, and hemorrhoids. Prebiotic fibers appear to enhance immune function. Dietary fiber intake provides similar benefits for children as for adults. The recommended dietary fiber intakes for children and adults are 14 g/1000 kcal. More effective communication and consumer education is required to enhance fiber consumption from foods or supplements.
Brittany, Thank you so much for leaving a comment! Without being there in the kitchen with you, it’s difficult to say what the issue was; however, I can definitely help you troubleshoot…did you cook it for the full amount of time the recipe calls for, and did you cover the top with foil for the last 15 minutes? If so, there might be an issue with your oven’s calibration (you can get an inexpensive oven thermometer to check this). Another tip is to let your eggs come to room temperature first. Another factor is the altitude at which you’re baking; if you’re at high altitude, you might need to slightly adjust the oven temperature and bake time. The other thing to remember is that there will usually be a little bit of fall to most keto breads (in fact, every keto bread we’ve ever made) because keto flours lack gluten and are naturally quite dense; however, you can see in the photos, we still got a good rise on this loaf. I hope these tips help!
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