Jump up ^ Klein MS, Buttchereit N, Miemczyk SP, Immervoll AK, Louis C, Wiedemann S, Junge W, Thaller G, Oefner PJ, Gronwald W (February 2012). "NMR metabolomic analysis of dairy cows reveals milk glycerophosphocholine to phosphocholine ratio as prognostic biomarker for risk of ketosis". Journal of Proteome Research. 11 (2): 1373–81. doi:10.1021/pr201017n. PMID 22098372.
Every recipe is less than 10 grams of carbs per serving. All recipes are gluten free and made only from whole, real, easy to find foods that you can find at your local grocery store. New resources are added to the plans each week. All the best information to help keep you on track with your low carb, keto lifestyle. I've even included a journal where you can track what you eat, how much you moved and how you are feeling overall. It is definitely the most comprehensive low carb meal plan out there. And for only $4.99 per week, you simply cannot beat the price.

It feels like everyone is talking about the keto diet — the high-fat, low-carb eating plan that promises to turn your body into a fat-burning machine. For that reason, keto has surged in popularity over the past year as a lose-weight-fast strategy. Thank Hollywood A-listers and professional athletes like Halle Berry, Adriana Lima, and Tim Tebow who’ve publicly touted the diet’s benefits, from shedding weight to slowing down aging. Here’s everything you need to know about going keto — and how to do it the Bulletproof way.


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.
So how does our body make ketones out of the stored fat?  First blood sugar and insulin have to be low enough to allow access to stored fat.  If they are, stored fat (in the form of triglyceride) can be mobilized as a fuel source. A substance called hormone sensitive lipase (HSL) breaks the triglyceride compound down into one glycerol molecule and 3 fatty acid molecules. These fatty acid molecules come in various lengths of carbon based chains.
The hypothalamus is the brain's main center responsible for hunger/satiety (H/S) control. In the theory that Mayer proposed more than 60 years ago, he assigned a central role to glucose levels in the H/S control: the so-called “glucostatic theory” (Mayer, 1955). Mayer suggested that depletion of carbohydrate availability leads to hunger, and the hypothalamic centers with receptors sensitive to glucose levels might be involved in the short-term regulation of energy intake (Mayer, 1955). The “feeding center” in the lateral hypothalamic area (LHA), according to the glucostatic theory, reacts to the between-meal fall of blood glucose and stimulates food intake. The LHA contains glucose-inhibited neurons that are stimulated by hypoglycemia, a process crucial to mediating the hyperphagia normally induced by hypoglycemia. The subsequent post-prandial hyperglycemia activates the “satiety center” in the ventromedial hypothalamus (VMH), which contains glucose-excited neurons and inhibits both “feeding center” and food intake.
Another product of elevated levels of free FA is polyunsaturated FA (PUFA). The potential ability of PUFA to block seizure activity in the brain is speculated to be associated with KD. Some mechanisms are thought to be a direct inhibition of voltage-gated sodium and calcium channels, modulation of a lipid-sensitive potassium channel, the activity of the sodium pump to limit neuronal excitability, or the induction of expression and activity of proteins in the mitochondria, thereby inducing a neuroprotective effect by partially inhibiting the production of reactive oxygen species (ROS) (Bough and Rho, 2007; Paoli et al., 2014).
Schele E., Grahnemo L., Anesten F., Hallen A., Backhed F., Jansson J. O. (2013). The gut microbiota reduces leptin sensitivity and the expression of the obesity-suppressing neuropeptides proglucagon (Gcg) and brain-derived neurotrophic factor (Bdnf) in the central nervous system. Endocrinology 154, 3643–3651. 10.1210/en.2012-2151 [PubMed] [CrossRef]
Glucose-sensitive neurons have been identified in a number of CNS regions including the metabolic control centers of the hypothalamus. Medeiros et. al. have used patch-clamp electrophysiology to examine whether neurons in a specific specialized region known as the subfornical organ (SFO), an area where the blood-brain barrier is not present, are also glucose sensitive or not. These experiments demonstrated that SFO neurons are glucose-responsive and that SFO is an important sensor and integrative center of circulating signals of energy status (Medeiros et al., 2012).
People (and even some ill-informed doctors) often confuse ketosis, which is a perfectly normal metabolic process, with ketoacidosis, which is a life-threatening condition. The latter is the consequence of insulin-deficient subjects having out-of-control blood sugar levels, a condition that can occur as well in alcoholics and people in a state of extreme starvation. Ketosis and ketoacidosis may sound vaguely alike, but the two conditions are virtually polar opposites and can always be distinguished from each other by the fact that the diabetic has been consuming excessive carbohydrates and has high blood sugar, in sharp contrast to the fortunate person who is doing Atkins.
Keto recipes that include nachos?! Oh yes. You’ll begin by making the fat head tortilla chips first. Did I mention you’ll use two types of cheese for this step? Delicious. Next, you’ll load them up with a meaty sauce and finish them off with your favorite toppings, like guac, salsa or sour cream. While these make a delicious snack, they’re frankly filling enough to share as a meal.

Hi Gigi, Low carb and keto is about the balance of macronutrients eaten (fat, protein and carbs), not specifically meat or lack thereof. Most people on keto do eat meat, though some people do vegetarian keto. Fat is actually necessary for many body processes. There is no issue for the kidneys with a high fat diet, but if you eat too much protein that isn’t great for the kidneys. It’s a common misconception that keto is high protein (it isn’t). Keto is great for diabetics as it naturally helps stabilize insulin. All of this being said, please know I’m not a doctor and you should consult your doctor on any medical questions or before starting any diet. If you have more questions that aren’t medical questions, I recommend our low carb & keto support group here.


Alison Moodie is a health reporter based in Los Angeles. She has written for numerous outlets including Newsweek, Agence France-Presse, The Daily Mail and HuffPost. For years she covered sustainable business for The Guardian. She holds a master’s degree from Columbia University’s Graduate School of Journalism, where she majored in TV news. When she's not working she's doting on her two kids and whipping up Bulletproof-inspired dishes in her kitchen.


If you’re looking to get a jump start on your health and fitness goals this year, you may be thinking about trying the ketogenic diet. Maybe you’ve heard the phrase before — it’s a huge diet buzzword — but aren’t sure what it means. Here’s a primer: The ketogenic diet is an eating plan that drives your body into ketosis, a state where the body uses fat as a primary fuel source (instead of carbohydrates), says Stacey Mattinson, RDN, who is based in Austin, Texas.
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