Brandi, Oh no, I’m sorry to hear about such a severe allergy! We carefully tested and re-tested this recipe and this is the best version we came up with. In order to come up with a recipe that doesn’t use coconut flour, we’d have to play around with not only alternative flours, but also adjust the amount of liquid (because coconut flour absorbs more liquid than most other flours), and additionally, potentially alter the bake temperature and bake time as well. I have a recipe for Paleo Sandwich Bread on my other blog that doesn’t use coconut flour that you might be interested in: I hope this is helpful!
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For a given quantity of fuel, the maximum amount of work that can be obtained from that fuel in a closed system is called ‘the Gibbs free energy’ (G). This takes into account the inherent ‘heat’ (combustion enthalpy (H)) and a property called entropy (a measure of tendency towards ‘disorder’ (S). The change in Gibbs free energy (∆G) is related to the change in combustion enthalpy (∆H), change in entropy (∆S) and the temperature (T):

I would like to point out that the metric conversion of 3/4 cup to 90g coconut flour as stated in your recipe is incorrect. Should be 84g per package labeling (Bob’s Red Mill). Unfortunately I made my first batch with 90g of coconut flour, and it was definitely not “pourable”. More like scoopable. I will try again with correct amount but thought I would point so you can update the recipe. Thank you!

We’ve now arrived at tip number 16. If you’re still having trouble losing weight, despite following the 15 pieces of advice listed above, it might be a good idea to bring out the heavy artillery: optimal ketosis. Many people stalling at weight plateaus while on a low carb diet have found optimal ketosis helpful. It’s what can melt the fat off once again.
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Moreover, in the above study of Sumithran et al. (2013), ketosis maintains post-prandial secretion of CCK as previously demonstrated by other researchers (Chearskul et al., 2008). Note that the orexigenic effect of BHB is blocked by transection of the common hepatic branch of the vagus nerve (Langhans et al., 1985). The hepatic branch contains fibers from the proximal small intestine, stomach and pancreas, and is sensitive to CCK (Horn and Friedman, 2004); ghrelin signals to brain are also transmitted via vagus nerve (Habara et al., 2014). Thus, the effects of ketosis on these two appetite-related hormones could be one of the many factors related to the effects of such nutritional regimen on food control.
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.
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.

In rats fed a ketogenic diet (Bio-Serv F3666) for 22 days, mitochondrial density (determined by electron microscopy) in the hippocampus increased in conjunction with increased transcription of 39 of the 42 mitochondrial proteins analyzed [162]. Similarly, mitochondrial content (mtDNA copy number) increased in skeletal muscle of mice fed a ketogenic diet (Research Diets D05052004; % energy: 89.5 fat, 0.1 carbohydrate, and 10.4 protein) for 10 months [163]. Higher mtDNA copy number was also observed in skeletal muscle of rats fed a high-fat, low-carbohydrate diet (% energy: 60 fat, 20 carbohydrate, and 20 protein) for 4 weeks in conjunction with daily injections of heparin (0.5 U/g) to increase circulation of fatty acids [87]. In humans, after just 3 days of a low-carbohydrate, high-fat diet (% energy: 50 fat, 34 carbohydrate, and 16 protein), fat oxidation significantly increased and 49% of the variance was explained by mtDNA content [79]. Despite this, the content of mtDNA did not change significantly, but this was expected given the brief duration of the diet.
For those, like myself, wanting a low-carb real bread I would recommend a proper low-carb yeast bread recipe with vital wheat gluten (the vast majority of people have zero gluten sensitivity, so the gluten-free fad is at best a waste and at worst a scam). Such breads have approx 1.5-2 grams more net carbs per 40g slice (5-6 grams total net carbs) than this recipe and I think it’s worth it.
Why is the keto diet good for you? A keto diet is one that prioritizes fats and proteins over carbohydrates. It can help reduce body weight, acne, and the risk of cancer. Find out about the mechanisms through which it achieves these benefits and the research that supports it. This MNT Knowledge Center article also discusses the risks of the diet. Read now
In order to simulate a bread-like texture without using gluten, grain free and gluten free bread recipes often use a variety of different flours and binders. We’ve tried so many keto bread recipes that taste way too eggy or too much like almonds or coconut. The trick is to find a combination of ingredients that yields good flavor, as well as bready texture and a loaf that rises nicely.