Hi there. The video didn’t show me draining the beef, because I didn’t. I use Butcher Box grass-fed beef, as noted and recommended in the recipe, which does not produce excess oil. While cooking, it is important to use your judgment while following a recipe and make changes that will suit you best. I am sorry this happened to you, and happy you have found an alternative method.
I have made this recipe several times now and my family loves it! Hubby is doing a weightloss program and this is really a treat for him. Freeze in popsicle molds and Kids love it too. I make them chocolate and they taste like fudgesicles. But the last two times its really grainy with the coconut fats in the milk after blending and freezing. The first few times it was perfect.Im pretty sure i used the same kind of coconut milk. Any idea what might be happening?? Thank you
Many questions about the role of such an important intermediate of lipid metabolism remains unanswered, e.g., the role of BHB in food control. For example, whether or not BHB could act as a satiety signal in the brain, considering its role in energy supply to CNS. We have to consider that the effects of KBs on hunger reduction can only be seen after many days following fasting or KD initiation (Paoli et al., 2010); this is consistent with the abovementioned threshold of brain utilization of KB as an energy source, i.e., 4 mmol/L (Veech, 2004), which is close to the Km for the monocarboxylate transporter (Leino et al., 2001). During the first days of fasting or KD there is a rise of BHB and adiponectin concentrations (Halberg et al., 2005). One of the putative causes of hunger in starved humans may be due—together with other causes—to adiponectin. When adiponectin binds to its receptor AdipoR1, AMP-activated protein kinase (AMPK) is phosphorylated in the ARC of the hypothalamus (Valassi et al., 2008). The increase of AMPK activity in the hypothalamus may increase food intake and hepatic glucose output in mice while the decrease seems to reduce food intake (Zhang et al., 2009). KDs can also act similarly to a caloric restriction on AMPK (Newman and Verdin, 2014). Interestingly, AMPK seems to have opposing actions on the liver, muscle tissues and the brain: in liver and muscle AMPK activation increases FA oxidation by decreasing malonyl-CoA concentrations (Malonyl-CoA is the first intermediate in the lipogenic pathway and is also an inhibitor of carnitine palmitoyltransferase-1 (CPT-1). CPT-1 activity can be limiting for FA oxidation), through the inactivation of the acetyl-CoA carboxylase 1 (ACC1). AMPK can also increase the activity of malonyl-CoA decarboxylase (MCD), which enhances the decrease of malonyl-CoA levels.
Still, it can be hard to get enough fat when you first start this diet. Butter, nuts, coconut and olive oils, and fatty cuts of meat are all on the menu. However, don't go overboard with polyunsaturated fats like soybean, corn, or sunflower oil. Keto dieters who increase their intake of those fats often end up with gastrointestinal distress that causes them to jump ship.
Achieving this state isn’t easy: You’ll need to severely minimize your intake of carbohydrates, eating no more than 20 to 50 grams (g) of carbs per day to get there and stay there. A single medium pear, for example, contains 26 g of carbs, and even foods that aren’t generally considered high in carbs — such as nuts and nonstarchy veggies — contain a small amount of carbohydrates, and so will need to be limited or avoided on this plan.
Following the ketogenic diet and achieving ketosis may be beneficial if you’re living with type 2 diabetes and need to manage your symptoms. Limiting carbohydrate intake is crucial with type 2 diabetes because too many carbs can increase blood glucose levels, which can damage blood vessels and lead to vision problems, kidney problems, and nerve problems.
Although the hunger-reducing effect of KD is well-documented, its main mechanisms of action are still elusive. The global picture is complicated by the contradictory role of ketosis on anorexigenic and orexigenic signals (summarized in Figure Figure4).4). Ketones (mainly BHB) can act both orexigenically or anorexigenically. In the orexigenic mechanism, it increases the circulating level of adiponectin, increasing brain GABA and AMPK phosphorylation and decreasing brain ROS production. The anorexigenic mechanism triggers a main normal glucose meal response, increasing circulating post-meal FFA (thus reducing cerebral NPY), maintaining CCK meal response and decreasing circulating ghrelin. It can be postulated that the net balance of the contrasting stimuli results in a general reduction of perceived hunger and food intake. More studies are needed to explore the mechanism of potential beneficial effects of KD on food control.
Meanwhile, the KD induces a ketosis that is not a pathological but physiological condition occurring on a daily basis. Hans Krebs was the first to use the term “physiological ketosis” despite the common view of it as oxymoron (Krebs, 1966); this physiological condition, i.e., ketosis, can be reached through fasting or through a drastically reduced carbohydrate diet (below 20 g per day). In these conditions, glucose reserves become insufficient both for normal fat oxidation via the supply of oxaloacetate in the Krebs cycle and for the supply of glucose to the central nervous system (CNS) (Felig et al., 1969; Owen et al., 1969) (Figure (Figure1).1). It is well-known that the CNS cannot use FAs as an energy source because free FAs cannot cross the blood-brain barrier (BBB). This is why the brain normally uses only glucose. After 3–4 days without carbohydrate intake (KD or fasting) the CNS must find alternative energy sources as demonstrated by Cahill et al. (Owen et al., 1967, 1969; Felig et al., 1969; Cahill, 2006). These alternative energy sources are the ketones bodies (KBs): acetoacetate (AcAc), β-hydroxybutyric acid (BHB) and acetone and the process of their formation occurring principally in the mitochondrial matrix in the liver is called ketogenesis (Fukao et al., 2004). Usually the concentration of KB is very low (<0.3 mmol/L) compared to glucose (≅ 4 mmol) (Veech, 2004; Paoli et al., 2010). Since glucose and KB have a similar KM for glucose transport to the brain the KB begin to be utilized as an energy source by the CNS when they reach a concentration of about 4 mmol/L (Veech, 2004), which is close to the KM for the monocarboxylate transporter (Leino et al., 2001).
“Keto is not easy to maintain, it’s not a palatable diet,” says Andrea Giancoli, a dietician and nutrition consultant in California. Getting 80-90 percent of your calories from fat—which is what’s generally required for keto—is actually difficult. It involves eating a lot of rich, heavy foods with little variety—think fatty meats and gravy on cauliflower. You’re only allowed 10 to 15 grams of carbohydrates per day, and though many dieters stretch that to more like 20 or 30 grams that’s still only about one banana. A single apple could also get you past that limit depending on its size (though the fiber in an apple means that many dieters don't count those carbs towards their daily limit) and a couple slices of bread likely fulfill the requirement as well.
Because people with type 2 diabetes are at an increased risk for cardiovascular disease, there’s a specific concern that the saturated fat in the diet may drive up LDL, or “bad,” cholesterol levels, and further increase the odds of heart problems. If you have type 2 diabetes, talk to your doctor before attempting a ketogenic diet. They may recommend a different weight-loss diet for you, like a reduced-calorie diet. Those with epilepsy should also consult their doctor before using this as part of their treatment plan.