Optimizing Inventory Management for Oilfield Service Companies
For oilfield service companies, optimizing inventory management is crucial for maximizing operational efficiency and profitability. In the past, manual processes and fragmented systems have posed challenges, resulting in inventory inefficiencies, lost productivity, and increased costs. However, implementing Discovery Management Solutions (DMS), an enterprise resource planning (ERP) system, can transform inventory management for oilfield service companies. This article explores how adopting DMS can revolutionize inventory management practices by focusing on key areas such as Centralized Inventory Control, Enhanced Demand Planning, Efficient Purchasing and Replenishment, Inventory Optimization, Warehouse Management, Batch and Lot Tracking, Integration with Field Operations, Improved Financial Management, Data Analytics and Reporting, and Compliance and Regulatory Support.
Centralized Inventory Control:
An ERP system provides oilfield service companies with the advantage of centralized inventory control. With DMS in place, businesses can consolidate inventory data from multiple locations and gain a comprehensive, real-time view of stock levels, locations, and movements. This centralized approach eliminates silos, reduces duplication, and prevents stockouts or overstock situations. By having a holistic inventory overview, organizations can make informed decisions, allocate resources efficiently, and reduce excess inventory carrying costs.
Enhanced Demand Planning:
Accurate demand planning is crucial for optimizing inventory levels and meeting customer requirements promptly. DMS offers powerful demand planning tools that analyze historical data, market trends, and customer forecasts to generate accurate demand forecasts. With this information, companies can align inventory levels with projected demand, minimizing stockouts and reducing inventory holding costs. Additionally, the integration of sales, marketing, and customer relationship management modules within DMS enables a holistic approach to demand planning, resulting in improved customer satisfaction and increased sales.
Efficient Purchasing and Replenishment:
Manual and fragmented purchasing and replenishment processes often present challenges for oilfield service companies. DMS streamlines these processes by automating purchase requisitions, generating purchase orders, and tracking supplier performance. By consolidating purchasing data and leveraging integrated workflows, businesses can enhance procurement efficiency, negotiate better terms with suppliers, and reduce lead times. Moreover, the system's ability to track supplier performance and maintain a centralized vendor database facilitates effective supplier management, ensuring timely deliveries and minimizing production disruptions.
Maintaining optimal inventory levels is an ongoing challenge for oilfield service companies. DMS offers advanced inventory optimization techniques, including economic order quantity (EOQ) and reorder point (ROP) calculations, which enable businesses to maintain optimal stock levels based on demand patterns, lead times, and cost considerations. Real-time inventory visibility allows organizations to reduce carrying costs, minimize stock obsolescence, and improve order fulfillment rates. Additionally, integration with sales and production modules enables automatic inventory updates, ensuring accurate stock availability information for customers and internal stakeholders.
Efficient warehouse management is crucial for oilfield service companies dealing with diverse inventory items and multiple warehouses. DMS provides robust warehouse management capabilities, including inventory tracking, put-away and picking strategies, bin management, and automated barcode scanning. These features streamline warehouse operations, minimize manual errors, improve order accuracy, and enhance productivity. By optimizing warehouse layout and implementing efficient picking strategies, businesses can reduce travel time, increase order throughput, and enhance overall operational efficiency.
Batch and Lot Tracking:
In a highly regulated environment, batch and lot tracking is essential for compliance and traceability purposes. DMS enables comprehensive tracking and traceability of inventory items, ensuring complete visibility into the movement of batches and lots throughout the supply chain. In the event of recalls or quality issues, businesses can quickly identify affected items, reduce response times, and mitigate potential risks. This level of traceability also helps in maintaining regulatory compliance and meeting audit requirements.
Integration with Field Operations:
Seamless integration between ERP systems and field operations is crucial for oilfield service companies relying on mobile field teams. DMS equipped with mobile capabilities allows field technicians to access real-time inventory data, update stock levels, and initiate requisitions directly from the field. This integration eliminates the need for manual data entry, reduces paperwork, and enhances overall productivity. Field technicians can also receive instant updates on stock availability and equipment availability, ensuring accurate service delivery and minimizing customer downtime.
Improved Financial Management:
Efficient inventory management directly impacts financial performance. DMS offers comprehensive financial management capabilities by integrating inventory data with accounting modules. This integration enables real-time cost tracking, accurate valuation of inventory, and improved financial reporting. By gaining insights into inventory costs, companies can make informed pricing decisions, assess profitability, and identify cost-saving opportunities. Moreover, automated financial processes such as invoicing, payment tracking, and reconciliation reduce errors, enhance cash flow management, and streamline financial operations.
Data Analytics and Reporting:
DMS empowers oilfield service companies with powerful data analytics and reporting capabilities. By leveraging integrated business intelligence tools, companies can generate real-time reports, dashboards, and key performance indicators (KPIs) related to inventory management. These insights enable businesses to identify trends, track performance metrics, and make data-driven decisions. With actionable information at their fingertips, organizations can proactively address inventory challenges, optimize supply chain processes, and drive continuous improvement.
Compliance and Regulatory Support:
Oilfield service companies operate in a heavily regulated environment, where compliance with industry standards and government regulations is paramount. DMS helps businesses adhere to compliance requirements by maintaining detailed records, generating audit trails, and facilitating accurate reporting. Whether it's tracking hazardous materials, maintaining safety certifications, or managing documentation related to inspections, DMS ensures that companies stay compliant, mitigating the risk of penalties or legal issues.
Implementing an ERP system offers numerous benefits to oilfield service companies, transforming their inventory management processes. From centralized inventory control and enhanced demand planning to efficient purchasing and replenishment, inventory optimization, and compliance support, ERP systems enable companies to streamline operations, reduce costs, and improve customer satisfaction. By harnessing the power of data analytics and integrated functionalities, oilfield service companies can achieve new levels of efficiency, agility, and profitability in their inventory management practices, gaining a competitive edge in the industry.


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Business Insights & Inspiration
Profile in Resilience: Meet Ann Hu
Shellee Fisher Davis Photographer
Ann Hu, a product/market manager at Cardinal Health, is profiled in the new Columbus area edition of The Women's Book's annually published directory of local inspiring women and resources that will be released on September 27, 2012. For the past two and a half years, Ann has been the company's presource product manager, overseeing the operating room (OR) accessories product segment.
The theme of our 2012 community directories is Resilience: Stories of Innovation & Inspiration. In our Columbus area directory, Ann shares her life story and advice about resilience:
“With resilience, I am able to sit back, reflect on failure or pain, regroup and pull myself out of the negative emotions. There are times in my life that I go through growing phases. Resilience helps me to break free from old habits, face my fear, and let go of control. Out of the inner turmoil and soul searching, come strength, confidence, and the realization of my dream.”
Join us for the Release Party to get your copy of the new book, hear an engaging panel discussion, and connect with our profiled women leaders and local resources for women.
We hope to see you there!


Being Coached: An Interview with the Author
By Lexie Ermi
Holly Williams, coaching founder and president of MAGUS Group, has penned a book called Being Coached: Group and Team Coaching from the Inside. Her years in the field of executive coaching provide her with the expertise and knowledge needed to competently write a book of this nature. Holly took the time to sit down with me and explain the impetus behind her desire to write a book and the impact she hopes the book will have on her readers.
"I wanted to write about how coaching lands on leaders and explain what it is liked to be coached," Holly explains. "I wanted the book to be inspiring for coaches who don't know how coaching lands on leaders and I also wanted leaders to see that it is not that intimidating to be coached."
My next question for Holly was, "What gave you the spark to create a model for group coaching to begin with?" She answers in detail, "Before I became a coach, I helped teams develop using drama improv methodology. After a few years of coaching executives with just the two of us in an office, I found that I missed the energy of a group of leaders all wanting to develop together. I love the way coaching works--with the leader being accountable for his/her development. So I started experimenting with coaching groups of leaders, and after a year had a great model that I have coached groups successfully with ever since!"
Holly went on to explain that there is no book on the market that fulfills the same goal as her new book. Most other books instead approach leadership coaching as a how to list of steps that must be achieved, using either case studies or purely expository writing to explain how to become a better leadership coach. The genesis of the book, Holly said, was having something to say about coaching and having a desire to put that across in a unique way. If a leader is curious about what it is like to be coached, this book will fulfill that need. It bridges the gap between leader and coach, making each more accessible to the other.
Being Coached is split into two parts. The first part covers group coaching and follows eight leaders, telling the story from their perspective. The second half covers team coaching with six executives who work together. The number of characters varies from chapter to chapter. Holly is working on another book that is similar in nature. It is about coaching and follows leaders in an organization who develop their coaching skills and how that plays out. "I might be done after this one – but who knows!" Holly explains.
"I was surprised by how much I truly enjoyed the writing process," Holly says. "I really enjoy writing and I think that comes across in the book. The book is a lot of conversation, just like coaching. That was the easy and fun part. The book really wrote itself. You know how people say the characters take over? That was the experience I had." While the writing was the easiest part, Holly goes on to say the hardest part was finding the time to actually write. Sitting down and writing for eight hours was impossible for her; instead, the process came about a lot more naturally by working a few hours every day in between her work that took up the normal day.
The whole book took two and a half years to write and publish. The barriers to publishing are lower than they have ever been because of things such as self-publishing. "It was tons of fun to have a hand in how the book would look and sound and feel. When you go with a mainstream publisher, you lose control of the book.
"My favorite part, besides the writing, is when people actually read it and talk about it with me. We've been getting reviews on Amazon and getting to read them – does it get any better than that?" Holly laughs.
Holly's book is sold on Amazon and we can look forward to her companion book, which she is currently in the process of writing, coming out in the future.
About Holly: Holly is a member of the Georgetown Institute for Transformational Leadership faculty, and her background includes leadership in a Fortune 50 Technology firm, as well as setting up business training programs for a Virginia community college. For over 15 years, her company has worked with executives and groups in business and government.
Being Coached is for sale on Amazon and will be available as a free Kindle download from Dec. 19-21, 2014.


Books and reading are a big part of who I am and a big part of what I bring to my consulting practice. From 2014 to early 2016, I maintained an active book-based blog called "What is Cathy Reading?" where I posted reviews and summaries of some of my favorites in leadership, personal growth, and business success. By clicking on each title below, you can link back to that blog, read a review, and download a summary. There are many more reviews posted at my Goodreads profile. Happy reading! And if there is something you've read that you think I will enjoy, please feel free to send me a note!


Published in Volume
108, Issue 6
(September 15, 2001)J Clin Invest.
Copyright © 2001, American Society for Clinical Investigation
Are natural killer cells the key to treating Epstein-Barr virus–associated lymphoproliferative disorders?
Bone Marrow and Stem Cell Transplantation Program, Division of Hematology and Oncology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA
Address correspondence to: Michael J. Robertson, Bone Marrow and Stem Cell Transplantation Program, Indiana University Medical Center, 1044 West Walnut Street, Room R4-202, Indianapolis, Indiana 46202, USA. Phone: (317) 274-6843; Fax: (317) 278-2262; E-mail: firstname.lastname@example.org.
Published September 15, 2001
Epstein-Barr virus (EBV) is a human herpes virus that infects predominantly oropharyngeal epithelial cells and mature B lymphocytes (1). Infection of epithelial cells by EBV results in replication of linear viral DNA, production of new virions, and lysis of the infected cell. In contrast, when B cells become infected by EBV, the virus can persist in a latent form and the cells can become immortalized and survive for the lifetime of the host. IgG antibodies specific for EBV, which indicate previous EBV infection, are found in the blood of more than 90% of adults. Primary EBV infection in children usually results in asymptomatic seroconversion or mild nonspecific symptoms, whereas about 50% of adolescents and adults with acute EBV infection experience infectious mononucleosis.
Primary EBV infection resolves without apparent clinical sequelae in virtually all immunocompetent people. CD8+ cytotoxic T lymphocytes (CTLs) appear to be crucial for control of the transformed B cells during primary EBV infection, although natural killer (NK) cells and other effector cells may participate in the immune response to EBV (1, 2). EBV-specific memory CD8+ T cells are believed to be primarily responsible for long-term in vivo suppression of latently infected B cells. EBV seropositive persons who become immunocompromised are at risk for the development of EBV-associated lymphoproliferative disorders (EBV-LPDs) (1, 2). EBV-LPDs have been observed in patients with HIV infection and patients on immunosuppression after allogeneic solid organ or hematopoietic stem cell transplantation. EBV-LPDs are clinically and pathologically heterogeneous (3, 4). A spectrum of histopathologic appearances, from polyclonal B cell hyperplasia to monoclonal diffuse aggressive B cell non-Hodgkin lymphoma, can be seen in EBV-LPD.
Treatment of EBV-LPDs is currently unsatisfactory. EBV-LPD regresses in some patients after the reduction or discontinuation of therapeutic immunosuppression (1, 2). However, this ap-proach exposes patients to risks of life-threatening organ failure or graft-versus-host disease (GVHD). Conventional chemotherapy and/or radiotherapy are sometimes effective but can be quite toxic in this clinical setting (5). In contrast, treatment with anti–B cell mAb’s appears to be very well tolerated (6, 7), although it may not be sufficient for patients with widely disseminated or more aggressive disease. Infusion of T cells from an HLA-compatible, EBV-seropositive donor can reconstitute EBV-specific immunity in immunocompromised recipients (8). Infusion of unfractionated donor leukocytes puts patients at risk for GVHD, however, and EBV-specific donor T cell lines (9) are arduous to prepare and are not widely available. Thus, novel therapeutic approaches are clearly needed for patients with EBV-LPD.
Lack of suitable animal models has been a major obstacle to the development of new treatments for EBV-LPD. However, the ability to reconstitute a human immune system in SCID mice offers a promising system for the study of this disease. Mature human T, B, and NK cells can persist and function in this mouse strain, which lacks endogenous T and B lymphocytes due to a defect in the recombinase system required for productive T cell receptor or immunoglobulin gene rearrangement (10). Injection of normal human peripheral blood lymphocytes (hu-PBLs) into SCID mice yields lymphohematopoietic chimeras, which have proved of value in studies of cancer and infectious diseases (11, 12). More recently, several groups have created hu-PBL-SCID chimeras using PBLs from EBV-seropositive donors and have shown that recipient mice reproducibly develop a fatal lymphoproliferative disorder of human B cells that resembles human EBV-LPD (13–15). The hu-PBL-SCID mouse would therefore appear to provide an excellent system in which to test immunotherapeutic approaches to EBV-LPD.
In this issue of the JCI, Baiocchi et al. (16) describe effective cytokine-based immunotherapy for EBV-LPD in this mouse model. Systemic administration of recombinant human GM-CSF and low-dose IL-2 was found to delay the development of EBV-LPD and prolong the survival of hu-PBL-SCID mice that were depleted of murine NK cells. The survival of hu-PBL-SCID mice treated with either IL-2 alone or GM-CSF alone was markedly inferior to that of mice treated with both cytokines (16) and was similar to that of animals treated with placebo (17). Experiments using PBLs depleted of various leukocyte subsets demonstrated that human NK cells, CD8 T cells, and monocytes contributed to the protective effect of IL-2 and GM-CSF. Moreover, an expanded population of EBV-specific human CD8+ T cells was detected in the spleens of hu-PBL-SCID mice treated with IL-2 and GM-CSF in combination, but not of mice treated with IL-2 alone. These results indicate that treatment with IL-2 and GM-CSF promotes the expansion of EBV-specific CD8+ T cells and suppresses the proliferation of EBV-transformed human B cells in vivo.
Several important issues are raised by the provocative findings of Baiocchi et al. (16). EBV antigen-specific CD8+ T cells have been thought to be the most important effectors for the control of EBV-transformed B cells (18), but the present data demonstrate a crucial role for NK cells in cytokine-based therapy for EBV-LPD. Without exception, animals depleted of both human and murine NK cells succumbed to EBV-LPD despite combined treatment with IL-2 and GM-CSF. Thus, the presence of NK cells is absolutely required for successful treatment of EBV-LPD in this model. In contrast, 20% of mice treated with both cytokines survived despite depletion of human CD8 T cells or monocytes. Currently it is not clear whether human NK cell–depleted mice fail to develop EBV-specific CD8+ T cells, which would suggest a requirement for NK cells in the afferent arm of the adaptive immune response. Alternatively, the animals may succumb to EBV-LPD despite the presence of antigen-specific T cells if NK cells are required along with CTLs in the effector phase of the immune response. One could begin to dissect the contribution of NK cells to the control of EBV-LPD in this model by evaluating their role in the afferent and efferent phases of EBV-specific CD8 T cell immunity.
The task of elucidating the role of NK cells in the hu-PBL-SCID model of EBV-LPD is complicated by the presence of functional murine NK cells in SCID mice (19). When hu-PBL-SCID mice are not depleted of murine NK cells, treatment with low-dose IL-2 alone is effective against EBV-LPD, and treatment with GM-CSF is not required (17). The mechanism whereby GM-CSF administration compensates for the absence of endogenous murine NK cells is not known and deserves further investigation. A clue may be offered by previous work of Baiocchi and Caligiuri (17), who found that successful treatment by low-dose IL-2 alone was associated with an accumulation of murine monocytes, murine NK cells, and human NK cells in peritoneal cavity of hu-PBL-SCID mice. Depletion of murine NK cells led to fatal EBV-LPD in 100% of IL-2–treated mice, whereas depletion of human NK cells had no effect. It seems reasonable to hypothesize that murine monocytes could interact productively with murine NK cells, but not human NK cells, in a protective response to EBV-transformed B cells. The accumulation of human monocytes as well as human NK cells in the peritoneal cavity of hu-PBL-SCID mice treated with both IL-2 and GM-CSF might compensate for the absence of murine NK cells in this system. Testing these hypotheses is conceptually straightforward and should shed further light on the mechanisms by which NK cells help to control EBV-LPD.
The attractive features of the hu-PBL-SCID experimental system should not blind one to its limitations (20). The immune defects that allow EBV-transformed B cells to proliferate unchecked in hu-PBL-SCID chimeras (15) may be very different from those of most immunocompromised humans. It is obvious, for example, that the human lymphocyte subsets that are adoptively transferred to SCID mice by injection of PBLs from healthy EBV-seropositive donors are not the same as the endogenous lymphocyte subsets of patients with advanced HIV infection. These issues become particularly acute when one wishes to use the results of hu-PBL-SCID experiments to design therapeutic approaches for human disease. For example, if GM-CSF in the hu-PBL-SCID model of Baiocchi et al. (16) is required merely to enhance the survival of injected human monocytes in the murine peritoneal cavity, administration of GM-CSF may not be necessary for the treatment of EBV-LPD in humans. Nevertheless, the results of Baiocchi and colleagues (16, 17) provide a solid foundation for further studies that can elucidate the mechanisms by which NK cells, monocytes, and CD8+ T cells contribute to the control of EBV-transformed human B cells in vivo. It is to be hoped that such preclinical studies will ultimately lead to more effective treatment for immunocompromised patients afflicted with EBV-LPD.
The author is supported in part by NIH grant MO1 RR00750-2753.
See the related article beginning on page 887.
Cohen, JI. Epstein-Barr virus infection. N Engl J Med 2000. 343:481-492.
Purtilo, DT, Strobach, RS, Okano, M, Davis, JR. Epstein-Barr virus-associated lymphoproliferative disorders. Lab Invest 1992. 67:5-23.
Knowles, DM, et al. Correlative morphologic and molecular genetic analysis demonstrates three distinct categories of posttransplantation lymphoproliferative disorders. Blood 1995. 85:552-565.
Orazi, A, et al. Posttransplantation lymphoproliferative disorders in bone marrow transplant recipients are aggressive diseases with a high incidence of adverse histologic and immunobiologic features. Am J Clin Pathol 1997. 107:419-429.
Mamzer-Bruneel, M-F, et al. Durable remission after aggressive chemotherapy for very late post-kidney transplant lymphoproliferation: a report of 16 cases observed in a single center. J Clin Oncol 2000. 18:3622-3632.
Fischer, A, et al. Anti-B-cell monoclonal antibodies in the treatment of severe B-cell lymphoproliferative syndrome following bone marrow and organ transplantation. N Engl J Med 1991. 324:1451-1456.
Kuehnle, I, et al. CD20 monoclonal antibody (rituximab) for therapy of Epstein-Barr virus lymphoma after hematopoietic stem-cell transplantation. Blood 2000. 95:1502-1505.
Papadopoulos, EB, et al. Infusions of donor leukocytes to treat Epstein-Barr virus-associated lymphoproliferative disorders after allogeneic bone marrow transplantation. N Engl J Med 1994. 330:1185-1191.
Rooney, CM, et al. Infusion of cytotoxic T cells for the prevention and treatment of Epstein-Barr virus-induced lymphoma in allogeneic transplant recipients. Blood 1998. 92:1549-1555.
Bosma, GC, Custer, RP, Bosma, MJ. A severe combined immunodeficiency mutation in the mouse. Nature 1983. 301:527-530.
Mosier, DE, Gulizia, RJ, Baird, SM, Wilson, DB. Transfer of functional human immune system to mice with severe combined immunodeficiency. Nature 1988. 335:256-259.
McCune, JM, et al. The SCID-hu mouse: murine model for the analysis of human hematolymphoid differentiation and function. Science 1988. 241:1632-1639.
Cannon, MJ, Pisa, P, Fox, RI, Cooper, NR. Epstein-Barr virus induces aggressive lymphoproliferative disorders of human B cell origin in SCID/hu chimeric mice. J Clin Invest 1990. 85:1333-1337.
Rowe, M, et al. Epstein-Barr Virus (EBV)-associated lymphoproliferative disease in the SCID mouse model: implications for the pathogenesis of EBV-positive lymphomas in man. J Exp Med 1991. 173:147-158.
Veronese, ML, et al. Lymphoproliferative disease in human peripheral blood mononuclear cell-injected SCID mice. I. T lymphocyte requirement for B cell tumor generation. J Exp Med 1992. 176:1763-1767.
Baiocchi, RA, et al. GM-CSF and IL-2 induce specific cellular immunity and provide protection against Epstein-Barr virus lymphoproliferative disorder. J Clin lnvest 2001. 108:887-894.
Baiocchi, RA, Caligiuri, MA. Low-dose interleukin 2 prevents the development of Epstein-Barr virus (EBV)-associated lymphoproliferative disease in scid/scid mice reconstituted i.p. with EBV-seropositive peripheral blood lymphocytes. Proc Natl Acad Sci USA 1994. 91:5577-5581.
Rickinson, AB, Moss, DJ. Human cytotoxic T lymphocyte responses to Epstein-Barr virus infection. Annu Rev Immunol 1997. 15:405-431.
Dorshkind, K, Pollack, SB, Bosma, MJ, Phillips, RA. Natural killer (NK) cells are present in mice with severe combined immunodeficiency (scid). J Immunol 1985. 134:3798-3801.
Tary-Lehmann, M, Saxon, A, Lehman, PV. The human immune system in hu-PBL-SCID mice. Immunol Today 1995. 16:529-533.


“Do you know how a fox gets rid of its fleas? The fox goes along the hedgerow, and collects little bits of sheep’s wool. Then he makes it all into a ball of wool, which he holds in his mouth. Then he goes to the stream, and slowly, slowly, walks down into the water. He lowers himself right down into the water, with the ball of wool in his mouth, until at last he is totally submerged; then he lets go, and ball of wool floats away downstream, carrying all the fleas with it. The fox merges, clean. In this image, Jesus is the ball of wool. The spotless Lamb allows the evil of the whole world to be concentrated on himself. He doesn’t keep it in circulation by reacting with violence; nor does he escape into the ineffective innocence of quietism. He takes the weight of the world’s evil upon himself, so that the world may emerge, clean.” (N.T. Wright, Following Jesus, p.48)
“God chose the human race to be the priests of all creation, offering up creation’s worship to Him and bringing His wise order to it. When humans sinned, God chose the nation of Israel to be the priests of the human race, offering up human praise and putting into operation God’s solution to the problem of sin. Israel herself, however, was sinful; God chose a family of priests (the sons of Aaron) to be priests to the nation of priests. The priests themselves failed in their task; God sent His own Son to be both priest and sacrifice. The inverted pyramid of priesthood gets narrower and narrower until it reaches one point, and the point is Jesus on the cross. The sacrifice of Jesus is the moment when the human race, in the person of a single man, offers itself fully to the Creator.”
–N.T. Wright, Following Jesus: Biblical Reflections on Discipleship (Grand Rapids: Eerdmans, 1994), p. 10.


From Volume 6, Issue 8 of MASS
Optimizing “Bulking Diets” To Facilitate Hypertrophy
by Eric Trexler, Ph.D.
Weight loss is a common goal for people who wish to improve their health, compete in a physique sport, or make weight for a strength sport with weight classes. However, weight gain is an equally valid and important diet goal, and should be approached just as strategically. This article discusses how to construct an optimized bulking diet.
A Concept Review of Optimizing Bulking Diets for Hypertrophy
The MASS archive has plenty of nutrition content related to fat loss, and for good reason. Fat loss is a common objective among the general population, whether the underlying goal is health-related or aesthetic in nature. Furthermore, fat loss is a critical aspect of physique sports, and a noteworthy consideration for all strength sports involving weight classes. Nonetheless, there are ample reasons to optimize one’s diet for hypertrophy facilitation rather than fat loss. Physique athletes have to get lean, but they won’t be going far in the sport without a sufficient amount of muscle for their competitive class. Many strength athletes need to make weight, but there’s no point in cutting weight classes if you don’t have the strength (and prerequisite muscle mass) to lift at a competitive level. Finally, there are some great reasons for general population folks to be interested in lean mass accretion. For many people with aesthetic goals, attainment of their dream physique will involve adding some amount of muscle mass, and there are noteworthy health benefits associated with increased strength and muscularity, particularly as we age. For this reason, it’s very common for people to take a cyclical approach to dieting, with “bulking” phases consisting of an energy surplus with a focus on muscle gain, and “cutting” phases consisting of an energy deficit with a focus on fat loss. Across a wide range of populations with varying fitness-related goals, there are many reasons to dedicate some time and attention to lean mass accretion, and a few key dietary adjustments and strategies can facilitate the process immensely. As such, the purpose of this article is to discuss how to optimize a “bulking” diet to maximally support hypertrophy.
Establishing an Energy Surplus to Facilitate Hypertrophy
It’s widely accepted that muscle hypertrophy is maximized in a state of positive energy balance. This describes a scenario in which the total amount of energy absorbed from the diet exceeds total daily energy expenditure, with the remainder of excess calories known as a caloric surplus or energy surplus. Despite the widespread acceptance of this idea, several questions persist. For example, why is an energy surplus advantageous? Is an energy surplus absolutely necessary for muscle growth in all circumstances? Exactly how large should an energy surplus be when hypertrophy optimization is the top priority? To achieve a deeper understanding of bulking diets, let’s dive into each of these questions.
Why is an energy surplus advantageous?
We can broadly categorize metabolic pathways as catabolic or anabolic. In catabolic pathways, energy-yielding nutrients (e.g., carbs, fats, proteins, and ketones) are broken down to yield energy-poor end products (e.g., carbon dioxide, water, and ammonia), and chemical energy (adenosine triphosphate, or ATP) is released in the process (1). For example, imagine that you begin exercising in a fasted state. Energy expenditure increases, and your body needs to break down some energy-rich substrates to adequately meet the rising demand for chemical energy (ATP). You’ll probably tap into a mixture of stored glycogen and stored fat, break them down to obtain ATP, and excrete the energy-poor end products of water and carbon dioxide. Greg gives an excellent overview of this process in a MASS article from Volume 1.
Anabolic pathways are the inverse of catabolic pathways. Rather than breaking down complex molecules into simpler end-products to extract energy, anabolic pathways involve building complex molecules (e.g., proteins, polysaccharides, lipids, and nucleic acids) from simpler precursors (e.g. amino acids, sugars, fatty acids, and nitrogenous bases), and chemical energy is actually required (used) to fuel the synthesis of these more complex end products (1). Muscle hypertrophy is an example of an anabolic pathway by which amino acids are assembled into muscle proteins, and ATP is required to power this process. Naturally, energy status is a critical regulator when it comes to both anabolic and catabolic pathways in the body. When demand for chemical energy exceeds the current supply, catabolic pathways are favored to liberate ATP. Intuitively, the body tends to scale down any unnecessary and energy-intensive anabolic pathways when catabolic pathways are being ramped up to solve an acute energy shortfall. Thus, at the surface level, we can see how maintaining a sufficient supply of accessible energy is an important factor dictating our capacity for muscle hypertrophy.
Is an energy surplus absolutely necessary for muscle growth?
I chose my words very carefully in the previous sentence: maintaining a sufficient supply of accessible energy is an important factor dictating our capacity for muscle hypertrophy. It’s important to recognize that “maintaining a sufficient supply of energy” goes beyond what you ate within the last few hours or maintaining positive energy balance over a given 24-hour period. We store enormous amounts of energy in adipose tissue; for example, we can access over 100,000 kcals of energy by breaking down 11kg of fat (2). As such, the concept of maintaining a sufficient supply of energy is intrinsically linked to a combination of long-term energy status (adiposity) and short-term energy status (the day-to-day relationship between energy consumption and energy expenditure).
If you’re looking for a specific formula that quantifies “overall energy status” based on acute energy balance and stored adipose tissue, you won’t find it here. We’ve got enough scientific evidence to understand that there’s an interplay between the two, and researchers have identified a number of mechanisms by which the body senses and keeps tabs on indicators of both short-term and long-term energy status. However, we don’t (to my knowledge) have the necessary information and depth of understanding required to construct a unified formula that comprehensively summarizes the balance of long-term and short-term energy status in a manner that would inform the promotion of muscle hypertrophy. Nonetheless, we have some very useful empirical observations that can inform actionable takeaways.
There is enough published research to render the following statement indisputable: it is possible to gain muscle mass without an energy surplus (3). In fact, it’s possible to gain muscle mass in a calorie deficit (4). However, it appears that adiposity is a major factor impacting the likelihood and magnitude of muscle gain in an energy deficit, which is also known as body recomposition. When long-term energy stores are high (e.g., we have plenty of stored body fat), it’s not particularly uncommon to observe noteworthy hypertrophy in the context of neutral, or even negative, energy balance. Conversely, recomposition is observed more rarely and in smaller magnitudes among individuals with very low body-fat levels. Another critical factor is the size of the energy deficit. As discussed in a previous MASS article, recomposition is routinely observed in the context of small energy deficits. However, as the energy deficit grows, the magnitude of hypertrophy increasingly tends to get blunted. A recent meta-regression (4) demonstrated that recomposition was quite common for calorie deficits up to around 200-300 kcal/day, but pretty atypical for calorie deficits larger than 500 kcal/day (Figure 2).
So, back to the original question: is an energy surplus absolutely necessary for muscle growth? Empirically, no. Hypertrophy is frequently observed in the presence of small-to-moderate energy deficits (3), and this is particularly true for people who have higher adiposity, less training experience, and a larger gap between their current level of muscularity and their maximal, genetically-determined limit for muscularity. However, there’s a more pertinent question for hypertrophy: is there a high likelihood of maximizing hypertrophy without an energy surplus? As reviewed by Slater and colleagues (5), evidence suggests that the answer is, “probably not.” Research indicates that an energy surplus is generally advantageous when the goal is to maximize the rate and magnitude of muscle hypertrophy, and this is likely related to the simple relationship between energy status and the facilitation of energy-intensive anabolic processes (and, by extension, the hormonal milieu associated with positive energy balance). Some folks are in a position where they can achieve meaningful hypertrophy in spite of neutral or negative energy balance, but positive energy balance appears to be ideal if an individual is solely and exclusively focused on maximizing hypertrophy.
Guidelines for calorie intake and rate of weight gain
Now that we’ve established the value of a positive energy balance, the next step is to determine how large of a caloric surplus is necessary. If the only goal is maximizing hypertrophy at all costs, then larger is generally better, but real-world scenarios typically aren’t that simple. If we overshoot the caloric surplus necessary to maximize hypertrophy, we invite completely unnecessary fat gain, which might be viewed as unfavorable (depending on the context).
In an excellent, open-access review paper, Slater and colleagues describe the multifaceted reasons for increasing calorie intake to support hypertrophy goals (5). As previously mentioned, ATP is used in the process of synthesizing new muscle proteins, so we need extra calories to support that energy cost. In addition, resistance training itself costs energy, and energy expenditure tends to remain transiently elevated for hours following an exercise bout. In addition, we need to supply the raw materials (amino acids) for new muscle proteins through dietary intake of protein, and these amino acids contain roughly 4kcal/gram, on average. As calorie intake increases, many individuals experience an adaptive increase in energy expenditure (6), which further increases their energy needs. This is analogous to metabolic adaptation; while underfeeding causes adaptive reductions in energy expenditure, overfeeding has a tendency to cause adaptive increases in energy expenditure. Finally, as you start accruing substantial amounts of muscle mass, total daily energy expenditure will increase further, as muscle mass is a metabolically active tissue that burns around 13 kcal/kg/day at rest (7), and even more so during exercise and non-exercise physical activity.
As outlined in the previous paragraph, we have a general idea of the factors driving increased energy needs for hypertrophy optimization. Unfortunately, there still isn’t much research identifying exactly how large a caloric surplus should be in order to maximally promote hypertrophy without driving unnecessary fat gain. Slater and colleagues recommend aiming for a calorie surplus of around 1500-2000 kj/day (359-478 kcal/day), which they classify as a “conservative” starting point. However, they acknowledge that this estimate is a very rough approximation, and that we don’t currently have the evidence required to establish a precise target or range. They further recommend to “closely monitor response to the intervention, using changes in body composition and functional capacity to further personalize dietary interventions.” By closely monitoring changes in body composition, the hypertrophy-focused lifter (or their coach) can quickly course-correct if the starting calorie target was too high or too low.
I think that’s a sensible recommendation, but you have to know your total daily energy expenditure in order to turn that recommendation into an actual daily calorie target. With that in mind, I’ll present three different methods for identifying one’s calorie target while bulking. As I described in a previous Stronger By Science article, I refer to the three strategies as 1) assume, 2) estimate, and 3) observe.
The “assume” approach is simple and straightforward: it assumes that one’s daily calorie target can be effectively dictated by their goal and current body weight. This strategy assumes that most people will generally maintain their current body weight if they consume roughly 15 kcals per pound of body mass. As a result, a general target for a moderate bulk would be around 17kcal/lb, and a general target for an aggressive bulk would be around 19 kcal/lb (Table 1). These bulking targets tend to work out relatively well for people with lower body weights (especially below 150lbs or so), but start to get excessively aggressive (in my opinion) once body weight starts climbing into the 200s and beyond. It’s also important to recognize that total daily energy expenditure can vary considerably from person to person, even if they weigh exactly the same. For these reasons, I do not recommend using the “assume” approach.
The “estimate” approach involves using validated equations to estimate one’s resting metabolic rate, then using activity factors to further estimate one’s total daily energy expenditure (TDEE). For a step-by-step guide through that estimation process, be sure to check out this article. In short, I recommend using the Cunningham 1980 equation to estimate resting metabolic rate based on fat-free mass (22 × fat-free mass [kg] + 500), and I recommend using the MacroFactor activity correction factors, which range from 1.2-1.6 for general (non-exercise) activity levels, and from 0-0.3 for the additive impact of structured exercise activity. Once TDEE is estimated, you’d aim to eat a certain percentage of that value in accordance with your goal. For example, someone with a maintenance goal would set a calorie target equal to 100% of TDEE, someone on a moderate bulk would aim for 105-110% of TDEE, and someone on an aggressive bulk would aim for 115-120% of TDEE (Table 2).
The “estimate” approach is great, and it’s certainly a viable strategy to use. However, I believe we can do better. The “observe” approach involves tracking your body weight every day (ideally measured immediately upon waking), while simultaneously tracking your daily caloric intake. After a couple weeks or so, you should be able to make very informative inferences about your energy needs. For example, if you’re consistently eating around 2400kcal/day and your bodyweight is very stable, then your maintenance calorie intake (and, by extension, TDEE) is around 2400kcal/day. If you’re slowly losing weight while consuming 2400kcal/day, then that intake is putting you in a small caloric deficit; if you’re rapidly gaining weight, then 2400kcal/day is putting you in a large caloric surplus.
While this approach requires a little more time and effort than the other two, it is 100% individualized and circumvents the need for imprecise heuristics or equations that rely on population-level averages. Once you get a decent idea of how your body weight is fluctuating in response to your current daily calorie intake, the goal is to adjust your calorie intake until you achieve an intended rate of weight change. If you have a previous history of successful bulking, you can also get a “head start” on the process – instead of monitoring how your weight is responding to your habitual, baseline level of calorie intake, you can jump straight to a calorie target that has worked in the past to determine if it’s still an appropriate target based on your body weight response. Someone with a maintenance goal would aim to keep body weight stable, while someone on a moderate bulk would aim to gain 0.1-0.25% of body mass per week, and someone on an aggressive bulk would aim to gain >0.25% of body mass per week (Table 3). However, it’s important to note that these categories might be a bit too conservative for people who are starting at lower body weights, so lighter individuals with lofty bulking ambitions should err toward the more aggressive side of these targets.
The “observe” approach is my personal favorite, and my default recommendation for two reasons. First, it’s completely individualized and requires the fewest possible assumptions. Second, it’s the only approach that has a built-in system for adjusting your calorie target over time. Once you identify an appropriate starting point for calorie intake, you continue to consistently monitor body weight to ensure that you’re staying on track with your intended rate of weight change. If you’re falling short of your weight gain goal, you’d increase your calorie target; if you’re exceeding your weight gain goal, you’d decrease your calorie target accordingly. This ongoing approach to calorie target adjustments is important because it directly accounts for changes in TDEE over time (which are to be expected), and allows the dieter to directly modulate their rate of weight gain in accordance with their current goal and comfort level (which could change over time). So, even if you use the “assume” or “estimate” approach to identify your initial calorie target, you’ll still want to begin monitoring weight changes to determine if this target is appropriate for you (and adjust it as needed). In other words, all roads should lead to the ongoing adjustment process implied by the “observe” approach if you intend to establish and maintain a goal-appropriate calorie target over time.
Throughout this section, I’ve mentioned bulking goals that fall on a spectrum. The most conservative approach is to aim for just slightly higher than maintenance calories (and, by extension, a slow rate of weight gain), while the most aggressive approach involves a very large surplus with a fast rate of weight gain. Choosing between a conservative, moderate, or aggressive approach will ultimately depend on a number of factors. If you’re a relatively inexperienced lifter, you can probably get away with a more aggressive approach to weight gain due to higher potential for substantial muscle growth. If you’re a very experienced lifter and near your genetic limit for muscularity, a more conservative approach would be advised, as substantial muscle gain is relatively unlikely. If your baseline weight is pretty low (relative to your goal), then you’ve got a lot of weight to gain, so a more aggressive approach is advised. If you’ve got a strong aversion to fat gain and are adamant about minimizing it, you’d want to go with a pretty conservative approach. Finally, if urgency is high and you’re in a major hurry to add muscle quickly, an aggressive approach would be your best bet.
Table 4 presents the different characteristics influencing bulking “category” selections (ranging from approximate maintenance to very aggressive). Each characteristic (training status, starting weight, aversion to fat gain, and urgency) falls on a spectrum, and it’s important to recognize that the bulking “categories” fall on a spectrum as well. For example, a moderate bulk might involve aiming for 105-110% of TDEE and an aggressive approach might involve aiming for 115-120% of TDEE, but someone with a “kind of aggressive” approach could certainly set their target directly between these two categories. Finally, it’s important to acknowledge that the different characteristics influencing category selection are, in some cases, uncorrelated. For example, a new lifter with minimal training experience should be capable of pretty rapid hypertrophy, but they might also have a major aversion to fat gain. Their training status suggests that an aggressive bulk could be a suitable option, but their aversion to fat gain would theoretically nudge them toward a more conservative approach. As such, the only way to maneuver this individualized decision-making process is to strike a balance between one’s circumstances and top priorities.
What is a Hardgainer?
It’s difficult to discuss bulking diets without acknowledging the concept of “hardgainers.” This colloquial fitness term refers to individuals who find it very challenging to gain weight, despite their best efforts. While some can’t even fathom the concept of struggling to gain weight, it’s a reasonably common thing in the lifting world. There isn’t a ton of research on people who are relatively resistant to weight gain, but a very recent paper (8) sheds some light on the topic. Hu and colleagues sought to explore and quantify some characteristics of people they describe as “healthy underweight” adults, meaning their BMI is naturally below 18.5 for reasons unrelated to eating disorders or any other medical conditions.
To achieve this objective, the researchers compared the weight-stable, healthy underweight adults (n = 150) to a control group of 173 weight-stable individuals with BMI values between 21.5-25. Due to smaller body size, the healthy underweight adults had lower values (in absolute terms) for resting energy expenditure and total daily energy expenditure. However, when scaled relative to their predicted energy expenditure values (which adjusts for body size), the healthy underweight participants had significantly higher resting and total energy expenditure, despite engaging in less physical activity and burning fewer calories from physical activity. The underweight individuals appeared to eat fewer calories than the normal weight control subjects in absolute terms, but they appeared to eat more total energy on a relative basis (scaled to body size). These findings suggest that higher-than-expected resting metabolic rates could contribute to weight gain resistance in naturally lean individuals. However, I am skeptical that this single characteristic tells the whole story, and I suspect that two additional factors can make it very challenging for an individual to intentionally gain weight.
As mentioned previously in this article, overfeeding can induce an increase in TDEE, largely by increasing non-exercise activity thermogenesis (6). However, the observed increase in TDEE varies considerably from person to person. In a 1999 study, Levine and colleagues fed volunteers an extra 1000kcal per day for eight weeks. Despite the standardized increase in calorie allowance, they found an enormous amount of variability in the amount of weight gained, with 10-fold differences separating the individuals with the most fat gain (4.23kg) from those with the least fat gain (0.36kg). Fat gain was inversely correlated with the increase in total energy expenditure (r = -0.86, p < 0.001) and the increase in non-exercise activity thermogenesis (r = -0.77, p < 0.001; Figure 3). This well-controlled study demonstrated that different individuals gain very different amounts of fat in response to identical calorie increases, and its results directly link overfeeding-induced increases in energy expenditure to resistance to fat gain (and total weight gain).
In summary, it’s very possible, if not likely, that many hardgainers are individuals who experience particularly large energy expenditure increases when they attempt to achieve a calorie surplus. This has important implications when it comes to setting a calorie target for a bulking diet. If a hardgainer tries to implement strategies that set calorie targets based on body mass or an estimated TDEE value (such as the “assume” or “estimate” approach), with no system in place to make incremental adjustments based on progress, they might find that their elevation in TDEE largely or entirely wipes out their planned surplus. This is yet another reason why I recommend the “observe” approach, which involves systematically adjusting your calorie target until a desired rate of weight gain is achieved. For hardgainers, the necessary level of calorie intake is often dramatically higher than expected. Imagine coaching some of the most weight-gain-resistant participants in Levine’s study – a well-planned increase of 1,000 kcal/day beyond maintenance needs, in a well-controlled intervention, yielded a minimum weight increase of only 1.4kg and a minimum fat mass increase of only 0.36kg across a two-month time period.
Aside from inter-individual differences in energy expenditure responses to overfeeding, I suspect that inter-individual differences in appetite regulation play a role as well. Back in Volume 3, we had an excellent guest article by Dr. Anne-Kathrin Eiselt (if you haven’t read it yet, I highly recommend it). In that review, Dr. Eiselt describes the multifaceted nature of hunger and satiety regulation, in addition to the complex relationship between the consumption and reward systems of the brain. In short, there are distinct areas of the brain in which we are constantly processing information related to hunger, satiety, and reward sensations. These centers are in a state of ongoing neuroendocrine communication and coordination, and the net balance of these coordinated interactions has a direct impact on one’s appetite and energy intake.
When it comes to hardgainers, I think it’s best to describe the relevance of these concepts within the context of the dual intervention point model, which Helms described in last month’s issue of MASS. Within the fitness industry, it’s common to suggest that each individual has a body-fat “set point,” or an individualized body-fat percentage that their body actively works to defend. When taken literally, this theory would suggest that every person’s hunger, satiety, and reward center control is finely tuned to keep them stuck at a single specific body-fat percentage, and any deviation from that exact level of adiposity requires a substantial amount of ongoing intentional effort to maintain. As explained by Speakman et al (9), that theory does a poor job of explaining weight regulation. A more suitable model suggests that each person has a range of body-fat levels in which they generally feel comfortable. An individual’s hunger, satiety, and reward center control systems are tuned to keep them within that broad range of adiposity, but their habits and behaviors dictate whether they’re near the top, middle, or bottom of their genetically predetermined range. As a person starts getting near the bottom end of their comfortable range, also known as their lower intervention point, they start to receive some significant physiological feedback to prevent them from getting leaner (such as increased hunger, reduced satiety, and reduced energy expenditure). As a person starts getting near the top end of their comfortable range, they receive some physiological feedback to prevent them from getting heavier (such as blunted hunger, increased satiety, and increased energy expenditure). The dual intervention point model is presented in Figure 4.
So, what does this all mean for hardgainers?
I suspect that many hardgainers exist in a “baseline state” that is quite close to their upper intervention point. For example, a hardgainer’s hunger and satiety circuitry might be wired in a way that sets their upper intervention point in a relatively “low” position, such that the slightest increase in body mass is met with a high degree of friction (in the form of a totally blunted appetite). This has a direct connection to the findings by Levine et al (6), who found that some non-obese individuals gained fat quite readily during overfeeding, while others were quite resistant to fat gain, despite falling in the same BMI range at baseline and receiving the same thousand-calorie increase beyond maintenance needs. We can imagine a very plausible scenario in which the weight-gain-resistant participants in Levine’s study were simply closer to their upper intervention point at the beginning of the study – not because they had dramatically higher adiposity levels, but because their genetically-determined upper intervention point was simply lower. This weight gain disadvantage can be overcome, but not without a focused and strategic effort.
Regardless of upper intervention point positioning, a hardgainer’s challenges might be exacerbated with a neurophysiological reward system circuitry that simply isn’t very responsive to hyperpalatable foods. As reviewed by Dr. Eiselt, hyperpalatable foods can cause robust neurophysiological reward responses that elicit a tremendous sensation of pleasure and enjoyment. However, a simple chat with your friends or family will make it very clear that different people have very different responses to food. Of course we all have specific flavor preferences that differ from one another, but upon closer examination, you’ll also find that the magnitude of pleasure derived from hyperpalatable food is quite variable from person to person. In fact, a growing body of evidence shows that the reward sensation, or magnitude of pleasure derived from eating, can vary over time and among different eating contexts (10), even for the same individual eating the same food. This is relevant to the plight of hardgainers, because stimulation of the brain’s reward system can override satiety cues, which directly enables intake of more calories. This is often viewed as the major “downside” of hyperpalatable foods within the context of weight loss, but robust reward responses to hyperpalatable foods are actually helpful when appetite is blunted during intentional weight gain.
In summary, hardgainers are individuals who struggle to induce intentional weight gain, and they certainly exist in considerable numbers. A number of factors might contribute to this difficulty, such as a higher-than-expected resting metabolic rate, an exaggerated increase in energy expenditure during overfeeding, or a balance of hunger and satiety regulatory circuits that generally lean toward a lack of appetite. Within the context of the dual intervention point model, we might view these individuals as having a baseline status that is already quite close to their upper intervention point, which makes it very difficult to sustainably increase body weight. It’s also quite possible that some hardgainers may simply experience blunted reward sensations in response to hyperpalatable food consumption, which might nudge them toward lower calorie intakes due to lack of interest and an inability to overcome satiety signals via pleasure and reward signaling.
Strategies for Hardgainers
On paper, the challenges faced by hardgainers are easy to solve. Set a suitable calorie target, and hit it consistently. If that calorie target fails to promote your intended rate of weight gain, incrementally increase your calorie target until you start gaining weight at the intended rate. If your weight gain slows or stalls entirely, incrementally increase your calorie target again. Easy stuff, in theory. In practice, it’s far more challenging. Many hardgainers carry out this incremental process of calorie target adjustment until they inevitably reach a major hurdle: due to extreme fullness and an absence of hunger, it becomes very difficult to reach the daily target for calorie intake.
Unfortunately, overcoming weight gain challenges isn’t commonly viewed as a major public health priority. With obesity prevalence exceeding 40% in the United States, weight loss has been prioritized extensively in the scientific literature. A great deal of research has been conducted for the purpose of identifying eating habits, patterns, and strategies that increase satiety and reduce hunger to facilitate passive weight loss. As reviewed in a previous MASS article, the evidence generally indicates that hunger can be attenuated by eating more slowly, eating more mindfully in the absence of distractions, avoiding hyperpalatable meals, and structuring meals with low energy density and plenty of unprocessed or minimally processed foods with harder textures. If we invert these findings, we can flip the satiety promotion literature to yield some very helpful strategies for satiety attenuation.
If appetite suppression is a major hurdle preventing a hardgainer from consistently consuming enough energy to gain weight, they’ll likely benefit from incorporating more energy-dense foods. These types of foods will provide a large number of calories while taking up less space on their plate (and in their stomach), which may confer both psychological and physiological advantages favoring increased energy intake. By opting for foods with a high degree of processing and softer textures, a hardgainer may be able to eat more quickly, which appears to facilitate higher calorie intakes before reaching a given satiety level (11). Selection of hyperpalatable foods appears to override some intrinsic satiety signals; this can be counterproductive for weight loss goals, but advantageous for hardgainers. If nothing else, hyperpalatable food selection gives hardgainers a more compelling reason to eat when appetite is low; a tasty meal is inherently rewarding from a neurophysiological perspective, whereas it’s often difficult to compel yourself to force down another plate of plain chicken, broccoli, and sweet potatoes. Finally, there is some evidence to suggest that energy-dense snacking can lead to increased calorie intake over time (12). While the snacking literature is a bit inconsistent (13), it appears that energy-dense snacking is associated with either no change or increases in body weight, and snacking lends itself to a more distracted, less mindful form of eating that could passively facilitate increased energy intake.
In summary, hardgainers who are struggling to hit their daily calorie target should aim to incorporate more foods with higher energy density, greater palatability, softer textures, and a higher degree of processing. Furthermore, meals should be supplemented with palatable, energy-dense snacks that can be consumed somewhat mindlessly throughout the day to encourage passive increases in energy intake. In other words, make a list of the most common hunger-fighting strategies for fat loss diets, then do the exact opposite.
Macronutrient Distribution While Bulking
Once a calorie target is selected, the next step is to address macronutrient distribution (after all, those calories have to come from somewhere). I’ll address protein first, because that’s the simplest of them all. The “standard” evidence-based protein recommendations will do just fine for bulking purposes, whether you’re taking a conservative or aggressive approach. There are some situations where these recommendations might require some adjustments, such as a scenario in which a very lean person is dieting pretty hard (14), but protein is very simple when energy balance is neutral or positive. As a result, individuals on a bulking diet are likely to fully optimize their hypertrophy progress by aiming for around 1.6-2.2 g/kg/day of protein (15), which should scale to roughly 2-2.75 g/kg of fat-free mass (rather than total body mass) per day. If those two different ranges give you very different protein intakes (which may be observed, depending on your weight and body composition characteristics), my recommendation is to scale your protein intake to fat-free mass rather than total body mass. Furthermore, you should split this daily protein target roughly evenly among 3-6 meals per day (one, two). If you want a hyper-optimized meal schedule that relies on a little bit of mechanistic speculation but leaves nothing to chance, you might consider restricting this even further, with an eating schedule that splits protein intake across 4-5 meals per day, with at least 2-3 hours between meals. However, a relevant note for bulkers: if you’re eating relatively low-protein snacks throughout the day to facilitate high daily calorie intakes, these low-protein snacks wouldn’t be counted as “meals.” In this context, a meal will generally provide at least 0.3g/kg of protein per day, or an absolute dose of at least 20-30g of protein.
When it comes to carbohydrate and fat intake, the conversation gets a little more interesting. First, I think it’s defensible to suggest that extreme carbohydrate restriction is generally inadvisable while bulking. Previous MASS articles have noted that ketogenic diets tend to have either similar or slightly worse effects on hypertrophy when compared to more balanced macronutrient distributions, and there is mechanistic evidence to suggest that maintaining an abundant supply of glycogen is generally favorable for lifters. In addition, a very recent meta-analysis indicates that carbs are ergogenic for lifters who complete training sessions that include plenty of maximal-effort sets and/or last longer than 45 minutes in duration (16). There are certainly some scenarios in which lifters can get by with very low carb intakes, but it’s hard to broadly suggest that extreme carbohydrate restriction is an optimal approach to bulking diets for lifters.
On the completely opposite end of the spectrum, some folks suggest that lifters should follow bulking diets with very high carb intakes and pretty aggressive fat restriction. The reasoning for this relatively common recommendation is based on a few distinct observations. First, there is evidence that carb overfeeding increases TDEE more than fat overfeeding (17). This means that a high-carb overfeeding diet would, calorie-for-calorie, lead to slightly less fat gain than a high-fat overfeeding diet, which has been observed in the published literature (18). Second, it has become fairly common knowledge that de novo lipogenesis (the process by which our bodies convert carbohydrate to fat for long-term storage) is rarely observed in real-world scenarios, such that de novo lipogenesis typically makes negligible contributions to the storage of additional fat mass (19). Many folks interpret this to mean that people who overshoot their calories on a high-carb bulking diet will neglect to store the excess calories as fat, thus allowing for an aggressively high calorie target without the risk of excessive fat storage. Third, proponents of this high-carb bulking strategy often point to a particular piece of empirical evidence that seems to lend support. An abstract published in 2011 seems, at the surface level, to suggest that high-carb, high-calorie bulking with aggressive fat restriction leads to more hypertrophy and less fat gain than a very similar diet with less aggressive fat restriction. While the abstract itself is hard to find these days, it was covered in an excellent write-up on the SuppVersity blog several years ago.
Personally, I am skeptical that high-carb bulking with extreme fat restriction is the “cheat code” that some proponents make it out to be. First, I’ll acknowledge that high-carb overfeeding does increase TDEE more than calorie-matched high-fat overfeeding (17), which is primarily due to the fact that carbs have a higher thermic effect of feeding than fat (18), particularly when consumed in large quantities. However, this isn’t necessarily an advantage in all contexts. If you’re perpetually hungry and looking for a more satiety-inducing diet while bulking, this might be a helpful and actionable observation, and you might consider opting for a relatively high-carb, high-fiber, high-protein approach. However, this is actually an extra challenge from the perspective of a hardgainer who’s struggling to consume enough calories to support weight gain. There is definitely a difference in the thermic effect of carb versus fat overfeeding, but whether or not that’s an advantage or disadvantage depends on the context, and the magnitude of the effect isn’t particularly large – for example, Dirlewanger et al (17) found that a 40% energy surplus (140% of TDEE) increased TDEE by about 140 kcal/day during high-carb overfeeding, whereas high-fat overfeeding increased TDEE by almost half of that. A similarly small difference between high-fat and high-carb overfeeding was observed by Horton et al (18), which suggests that this difference is more interesting than it is impactful.
Next, it’s important to contextualize the claim that de novo lipogenesis is rarely observed in real-world applications, to the extent that we can largely disregard its role in the maintenance of human fat stores. It is true that “real-world scenarios” (that is, diets with relatively balanced macronutrient contents) generally don’t lead to meaningful amounts of de novo lipogenesis. For example, an overfeeding study by McDevitt et al (19) concluded that de novo lipogenesis “does not contribute greatly to total fat balance,” and the results of an overfeeding study by Horton et al (18) indirectly suggest that de novo lipogenesis did not occur to an extent that would meaningfully impact total fat storage. However, there’s a huge caveat to keep in mind with these studies: fat intake was not aggressively restricted. De novo lipogenesis is a convoluted and energetically costly pathway. As a result, the human body prefers not to use it unless it’s actually necessary. If you’ve got tons of carbohydrate and fat available after a meal, your body is inclined to take the easiest and most efficient path, which involves burning the carbs for immediate energy and storing the fat for later use.
It’d be hard to justify the process of converting extra carbs to fat for storage while you’re simultaneously burning fat to meet immediate energy demands – a more straightforward and energy-efficient strategy is to store the stuff that’s already in a storable form (the dietary fat from the previous meal). To draw on an analogy, imagine that I owe you $20USD and you owe me $15USD. It would be possible for me to pay you $20USD and request that you mail me $15USD worth of Euros, which I could then take to the bank, convert back to USD, and deposit into my account. Or I could just give you five bucks.
Your body is more than capable of converting extra carbs to fat for storage if absolutely necessary, and if you’ve got a huge surplus of carbs and fully saturated glycogen stores, that’s exactly what will happen. In a high-carb overfeeding study, Acheson et al (20) implemented a multiple-day glycogen depletion protocol, followed by 7 days of high-carb overfeeding. Notably, fat intake was aggressively restricted to only 3% of total energy. In short, the extra calories were handled exactly how you’d expect them to be handled. At first, a bunch of the carbs were allocated toward refilling the recently depleted glycogen stores. Once glycogen stores were topped off, participants had to deal with a huge surplus of calories that were almost exclusively coming from carbohydrates. Even after sending the small amount of dietary fat straight to storage and burning carbs to meet immediate energy needs, there were still a ton of carbs left over. As a result, the participants used the de novo lipogenesis pathway to convert the carbs to fat and store the extra energy for later. As a result, the researchers concluded that glycogen stores “can accommodate a gain of approximately 500 g before net lipid synthesis contributes to increasing body fat mass.”
In summary, it’s true that de novo lipogenesis is pretty negligible in most real-world scenarios and nutrition studies. However, that’s mostly because real-world scenarios and nutrition studies rarely involve massive amounts of carbohydrate overfeeding combined with aggressive fat restriction. When possible, the default preference of the human body is to allocate extra dietary fat toward storage and to burn extra dietary carbohydrate. For example, imagine a scenario in which you’ve overshot your energy surplus a bit, and you’re eating an extra 300 kcal/day beyond the energy needed to support muscle growth. If you’re eating 80g of fat per day (which is 720 kcal/day from fat), the path of least resistance is to simply store 300kcal worth of the dietary fat that was consumed. However, if we try to “cheat the system” by creating a bulking scenario in which our leftover energy greatly exceeds our glycogen storage capacity and daily fat intake, the extra calories from carbs aren’t going to disappear – we’re more than capable of converting them to fat and storing them.
So, my carb and fat guidelines for bulking are pretty simple: get at least 3-4g/kg/day of carbohydrate, and calculate your daily fat minimum (in grams) by subtracting 150 from your height (in cm), then dividing the outcome by 2, and adding 30. So, someone who is 180cm tall would have a daily fat minimum of (180-150)/2 + 30, which equals 45g/day. If you’re under 150cm tall, you probably want to ignore this equation and set your lower boundary to a default value of 30g/day. These guidelines should help to ensure that most dieters are getting enough carbohydrate to fuel their training and enough fat to support good health. Notably, these guidelines are bare minimums, and bulking diets tend to involve pretty high calorie targets, which means you have a ton of wiggle room to work with. As long as you’re meeting or exceeding the bare minimums for carb and fat intake, their exact ratio is pretty inconsequential while bulking, so you should feel free to eat in accordance with your preferences.
Should I Bulk, Cut, or Recomp?
For the huge number of folks whose goal physique involves more muscle and less fat mass, it can be challenging to construct a plan for tackling these distinct subgoals. When determining if the best immediate course of action should involve bulking, cutting, or trying to achieve recomposition, it’s hard to provide a generalizable answer for everyone. However, there are some answers that we can categorize as generally inadvisable.
Some folks might answer by indicating that recomping is virtually impossible, then nudging you toward a large energy deficit or a large energy surplus. As we’ve already covered, this isn’t true, and it’s especially untrue for people with high levels of adiposity or relatively minimal training experience. As such, there are some folks who might wish to begin by recomping rather than bulking or cutting, whereas others might opt for a sequential, multi-step approach that starts with a dedicated phase to explicitly focus on either fat loss (cut) or muscle gain (bulk). As noted previously, some people can also “split the difference” – if you can’t decide between cutting or recomping, you can just do a very conservative cut and try to get the best of both worlds. Similarly, if you’re torn between bulking or recomping, you can just do a very conservative bulk.
Some folks might answer by indicating that you should cut first, because weight loss will potentiate future hypertrophy by enhancing insulin sensitivity or reducing basal inflammation levels. This response is tied to the concept of p-ratios, which was first proposed by Forbes as a way to model relative changes in fat mass and fat-free mass among people who do not lift weights (21). If you’re new around here, this is a topic I’ve covered extensively – first as a MASS article, and then as a 3-part Stronger By Science article series (one, two, three). Needless to say, there’s plenty of content to dig into if you’d like to explore this topic in detail. The short version of the conclusion is that this p-ratio concept has minimal relevance to people who are regularly lifting weights, and the overwhelming majority of evidence in lifters contradicts the idea that getting leaner will increase the magnitude or rate of hypertrophy achieved during a subsequent bulk. In fact, we did our own participant-level meta-analysis with full data sets from seven different resistance training studies, resulting in complete data from over 160 study participants. We created a “lean gains” metric, which is simply the change in fat-free mass minus the change in fat mass, and found that leanness did not confer the theoretical advantage implied by the p-ratio concept (Figure 5).
After digging deeper into the data, it became clear that participants with lower and higher body-fat percentages were achieving similar magnitudes of hypertrophy, whether you’re looking at changes in fat-free mass or direct measurements of muscle thickness. The primary difference was that individuals with higher baseline body-fat levels were more likely to lose a little bit of fat during resistance training interventions, but they were still able to achieve substantial hypertrophy in the absence of fat gain, or even in the presence of simultaneous fat loss. Thus, we concluded that getting leaner does not potentiate hypertrophy in a subsequent bulk, and that people with higher baseline body-fat are more capable of recomping. If anything, you could justify speculating that individuals with higher body-fat levels had slightly greater capacity for hypertrophy, given that they achieved similar amounts of hypertrophy in spite of less positive energy balance (as demonstrated by the tendency for fat loss).
A third inadvisable answer would encourage an individual (whose long-term goal involves being very lean) to get to a very low body-fat level (<10% body-fat for males, or <18% body-fat for females), then bulk from there while maintaining their hard-earned leanness. The participant-level analysis from our p-ratio article found that every single person under 8% body-fat at baseline had some degree of fat gain in the seven resistance training studies for which we had subject-level data, and only one of these individuals gained more than 1kg of fat-free mass. Based on these observations, in addition to the broader body recomposition literature (3), the probability of a very lean person gaining meaningful amounts of muscle mass without some degree of concomitant fat gain appears to be fairly low, which defeats the purpose of getting shredded on the front end of a bulk.
When deciding to bulk, recomp, or cut (and, by extension, how aggressively to bulk or cut), a lifter should consider several factors. As listed in Table 4, they should first reflect on their training status, starting weight, aversion to fat gain, and urgency. In doing so, they might clarify their own priorities well enough to make their decision quite easily. If not, I can offer my own perspective on how to navigate this dilemma. There are definitely some folks who feel that their starting level of adiposity is very incompatible with their day-to-day aesthetic goals, or contributing to some cardiometabolic health markers that are currently outside of their preferred ranges. If you’re starting in a spot where weight gain has a high probability of fueling some mild dissatisfaction related to body image, or ongoing concerns related to cardiometabolic health, then starting with a cut makes all the sense in the world (as a side note, it’d be a good idea to address any severe instances of body image dissatisfaction with a qualified mental health professional).
However, for lifters who are comfortable with their current body-fat level, generally fine with a little bit of additional fat gain, and know they want to gain a considerable amount of muscle over the remainder of their lifting journey, my general preference is to err toward bulking first and cutting later. Anecdotally, my observation is that many lifters’ “ideal body-fat level” (based on their personal goals and preferences) is either close to or below their lower intervention point (Figure 4). This means that the later stages of the cutting process is likely to get pretty tough, and the likelihood of sustaining that level of leanness during a subsequent (presumably conservative) bulking phase is fairly unlikely. I’ve also noticed that many folks who take the “cut first, bulk later” approach tend to be a bit dissatisfied with the results of their first cut. They often feel more “thin” and less “shredded” than they initially anticipated, largely because they underestimated exactly how much muscularity is required for a physique to have a “shredded” appearance. Furthermore, if their “ideal body-fat level” is absolutely shredded, or substantially below their lower intervention point, it’s quite likely that hypertrophy might be impaired. As noted previously, our p-ratio analysis seemed to indicate that it’s very hard to make lean gains at low body-fat levels.
With these considerations in mind, it’s very possible that a “cut first” approach could lead to some initial dissatisfaction when the initial cut is complete, and could also make the long-term goal striving process a little more challenging and a little more uncomfortable than it needs to be. However, that doesn’t mean it’s always a bad plan. For example, you might have a client whose lower intervention point is around 10% body-fat, would like to eventually be as lean as they can sustainably maintain, and generally dislikes to get above 16% body-fat while bulking (based on their personal aesthetic or health-related preferences). If they’re currently around 18% body-fat, it would be very defensible to cut to around 12-13% body-fat (comfortably above their lower intervention point), bulk until they reach about 15-16%, then oscillate back and forth between cutting and bulking phases until they’ve reached their ideal level of muscularity. At that point, they can cut down to around 10-11% body-fat as a reasonably comfortable maintenance range that is just above their lower intervention point. If they wish to be extra lean for certain special occasions (like a wedding, vacation, photo shoot, competition, etc.), they can temporarily cut down to a leaner body-fat level for a brief period of time, then settle back to their comfortable maintenance level when the special occasion has passed.
In summary, there are many factors to consider when deciding to bulk, cut, or recomp, and there is no one-size-fits-all approach. It’s important to thoughtfully reflect on individualized factors related to one’s hypertrophy potential, short-term priorities, and long-term goals prior to making a decision. Furthermore, the decision about where to start is, by definition, just the beginning. A lifter is likely to be consistently bouncing between short-term recomping, bulking, and cutting phases throughout the entirety of their fitness journey. So, with that in mind, don’t overthink the decision too much – the impact on body composition will become functionally irrelevant as enough time passes and a lifter shifts from phase to phase. The only way to totally screw this decision up is to choose a path that stifles a lifter’s ability to enjoy the process. Anything that stifles enjoyment or enthusiasm early in a lifter’s fitness journey has the potential to thwart motivation and derail the entire process.
One Last Thing – What About Cardio?
This article is getting pretty long, but there’s one last topic I’d like to briefly address before wrapping things up. A common misconception is that bulking necessarily requires an intentional avoidance of cardio and other non-lifting physical activity. On the surface, it’s an intuitive conclusion – people who are struggling to achieve an energy surplus aren’t eager to increase their energy expenditure, and many people are at least vaguely aware of the “interference effect,” which describes the attenuation of resistance training adaptations caused by concurrent cardio training. Fortunately for people who enjoy non-lifting physical activity (or simply value its health benefits), bulkers don’t necessarily need to avoid cardio at all costs.
First, let’s address the interference effect. This is a topic that’s been covered numerous times in MASS, so I’ll simply restate the main conclusions here. It is very true that studies have observed an attenuation of resistance training adaptations when cardio is added to the mix. However, this interference is far more pronounced for power adaptations than strength adaptations, and even less pertinent to hypertrophy adaptations. Furthermore, the cardio “dose” required to meaningfully interfere with resistance training adaptations tends to be pretty large (e.g., pretty arduous sessions at least 5-6 days per week). As Greg highlighted in one of his Research Briefs, the interference effect isn’t quite as scary as some make it out to be, especially for people with hypertrophy-focused goals and light-to-moderate doses of weekly cardio training.
In contrast to the large amounts of cardio required to meaningfully attenuate hypertrophy, noteworthy health benefits can be obtained from very modest amounts of cardio or non-lifting physical activity. For example, walking a mere 8,000 steps per day has been associated with a sizable reduction in all-cause mortality (22). In addition, the US guidelines for physical activity call for for 150-300 weekly minutes of exercise at “moderate” MET levels (3.0-5.9 METs), 75-150 weekly minutes of exercise at “vigorous” MET levels (≥6.0 METs), or a combination of the two. For context, some household chores like sweeping the floor or “general kitchen activity” are above 3 METS (i.e., in the “moderate” category), and a very brisk walk (4.5mph) can get you into the “vigorous” category (23).
In summary, a relatively small amount of cardio is needed for meaningful health benefits, and a very large cardio dose is needed to meaningfully interfere with hypertrophy adaptations. As a result, the typical bulker who’s doing non-lifting physical activity for the purpose of enjoyment or general health is unlikely to be racking up cardio doses large enough to impair hypertrophy. Similarly, they’re unlikely to be racking up cardio doses large enough to dramatically increase TDEE, so a little bit of extra activity shouldn’t make it prohibitively difficult to establish an energy surplus large enough to support hypertrophy. In conclusion, a successful bulk does not necessarily require that individuals alter their cardio or non-lifting physical activity habits. As long as you’re able to consume a suitable amount of calories and you aren’t doing cardio doses that resemble a highly competitive endurance athlete, additional physical activity should be pretty irrelevant.
While recomposition is definitely possible in a variety of circumstances, the majority of lifters will eventually find themselves in a position where a dedicated bulking phase is warranted to optimize hypertrophy. The first priority when bulking is to establish a state of positive energy balance (i.e., a calorie surplus), as extra energy is needed to accommodate the energy cost of building and maintaining new muscle tissue. It’s certainly important to get enough protein while bulking (1.6-2.2g/kg of body mass, or 2-2.75g/kg of fat-free mass), but the ratio of carbohydrate to fat in the diet is highly flexible. For many individuals, bulking is a fairly manageable process of estimating one’s total daily energy expenditure, setting a calorie target, and adjusting it to maintain the intended rate of weight gain. However, there are many hardgainers who run into considerable friction while bulking, which may be related to elevated resting metabolic rate, exaggerated increases in energy expenditure, inter-individual differences in hunger and satiety regulation, or blunted reward responses to hyperpalatable food. We can conceptualize hardgainers as being near their “upper intervention point” at baseline, and they may need to lean on dietary strategies that completely invert the guidelines that would typically increase satiety and reduce hunger. Bulkers need not worry about getting lean before their bulk or aggressively restricting their non-lifting physical activity, but they should carefully consider their current circumstances and priorities when deciding when (and how aggressively) to bulk.
- Ferrier DR. Biochemistry (6th ed). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2014:91-93.
- Hall KD. What Is The Required Energy Deficit Per Unit Weight Loss? Int J Obes. 2008 Mar;32(3):573–6.
- Barakat C, Pearson J, Escalante G, Campbell B, De Souza EO. Body Recomposition: Can Trained Individuals Build Muscle and Lose Fat at the Same Time? Strength Cond J. 2020 Oct;42(5):7–21.
- Murphy C, Koehler K. Energy Deficiency Impairs Resistance Training Gains In Lean Mass But Not Strength: A Meta-Analysis And Meta-Regression. Scand J Med Sci Sports. 2022 Jan;32(1):125-137.
- Slater GJ, Dieter BP, Marsh DJ, Helms ER, Shaw G, Iraki J. Is an Energy Surplus Required to Maximize Skeletal Muscle Hypertrophy Associated With Resistance Training. Front Nutr. 2019;6:131.
- Levine JA, Eberhardt NL, Jensen MD. Role Of Nonexercise Activity Thermogenesis In Resistance To Fat Gain In Humans. Science. 1999 Jan 8;283(5399):212–4.
- McClave SA, Snider HL. Dissecting The Energy Needs Of The Body. Curr Opin Clin Nutr Metab Care. 2001 Mar;4(2):143–7.
- Hu S, Zhang X, Stamatiou M, Hambly C, Huang Y, Ma J, et al. Higher Than Predicted Resting Energy Expenditure And Lower Physical Activity In Healthy Underweight Chinese Adults. Cell Metab. 2022 Jul 14; ePub ahead of print.
- Speakman JR, Levitsky DA, Allison DB, Bray MS, Castro JM de, Clegg DJ, et al. Set Points, Settling Points And Some Alternative Models: Theoretical Options To Understand How Genes And Environments Combine To Regulate Body Adiposity. Dis Model Mech. 2011 Nov;4(6):733.
- Rolls ET. Reward Systems in the Brain and Nutrition. Annu Rev Nutr. 2016 Jul 17;36:435–70.
- de Graaf C, Kok FJ. Slow Food, Fast Food And The Control Of Food Intake. Nat Rev Endocrinol. 2010 May;6(5):290–3.
- Tey SL, Brown RC, Gray AR, Chisholm AW, Delahunty CM. Long-Term Consumption Of High Energy-Dense Snack Foods On Sensory-Specific Satiety And Intake. Am J Clin Nutr. 2012 May;95(5):1038–47.
- Njike VY, Smith TM, Shuval O, Shuval K, Edshteyn I, Kalantari V, et al. Snack Food, Satiety, and Weight. Adv Nutr. 2016 Sep;7(5):866–78.
- Helms ER, Zinn C, Rowlands DS, Brown SR. A Systematic Review Of Dietary Protein During Caloric Restriction In Resistance Trained Lean Athletes: A Case For Higher Intakes. Int J Sport Nutr Exerc Metab. 2014 Apr;24(2):127–38.
- Morton RW, Murphy KT, McKellar SR, Schoenfeld BJ, Henselmans M, Helms E, et al. A Systematic Review, Meta-Analysis And Meta-Regression Of The Effect Of Protein Supplementation On Resistance Training-Induced Gains In Muscle Mass And Strength In Healthy Adults. Br J Sports Med. 2018 Mar;52(6):376–84.
- King A, Helms E, Zinn C, Jukic I. The Ergogenic Effects of Acute Carbohydrate Feeding on Resistance Exercise Performance: A Systematic Review and Meta-analysis. Sports Med. 2022 Jul 9; ePub ahead of print.
- Dirlewanger M, di Vetta V, Guenat E, Battilana P, Seematter G, Schneiter P, et al. Effects Of Short-Term Carbohydrate Or Fat Overfeeding On Energy Expenditure And Plasma Leptin Concentrations In Healthy Female Subjects. Int J Obes Relat Metab Disord. 2000 Nov;24(11):1413–8.
- Horton TJ, Drougas H, Brachey A, Reed GW, Peters JC, Hill JO. Fat And Carbohydrate Overfeeding In Humans: Different Effects On Energy Storage. Am J Clin Nutr. 1995 Jul;62(1):19–29.
- McDevitt RM, Bott SJ, Harding M, Coward WA, Bluck LJ, Prentice AM. De Novo Lipogenesis During Controlled Overfeeding With Sucrose Or Glucose In Lean And Obese Women. Am J Clin Nutr. 2001 Dec;74(6):737–46.
- Acheson KJ, Schutz Y, Bessard T, Anantharaman K, Flatt JP, Jéquier E. Glycogen Storage Capacity And De Novo Lipogenesis During Massive Carbohydrate Overfeeding In Man. Am J Clin Nutr. 1988 Aug;48(2):240–7.
- Forbes GB. Lean Body Mass-Body Fat Interrelationships In Humans. Nutr Rev. 1987 Aug;45(8):225–31.
- Paluch AE, Bajpai S, Bassett DR, Carnethon MR, Ekelund U, Evenson KR, et al. Daily Steps And All-Cause Mortality: A Meta-Analysis Of 15 International Cohorts. Lancet Public Health. 2022 Mar;7(3):e219–28.
- Ainsworth BE, Haskell WL, Herrmann SD, Meckes N, Bassett DR, Tudor-Locke C, et al. 2011 Compendium Of Physical Activities: A Second Update Of Codes And MET Values. Med Sci Sports Exerc. 2011 Aug;43(8):1575–81.


Someone please print this and take it up to her house and read it to her. Thank you in advance.
Its okay for you to go. Its okay for you to die and go to Heaven to be with your Savior who you worship with every breath you take and to be with Pappy, who is your true and never-ending love. I tried to tell you that you could go while I was with you a month ago, but I couldn't say the words. I loved rubbing your thumb and feeling you pat my arm way too much. Daddy told me that I needed to give you permission to leave, but I just couldn't. I love you so so so much and I have begun to mistake my breathtaking love for you for needing to have you here and that has turned into selfishness. Please go. You will be whole in heaven and you will be free from the body that is failing you here on earth. And I will see you again, so I must hold onto that.
I know that I have told you before that I am terrified for you to leave me, and I am. Who will love me with the massive unconditional force that your love is in my life? Who's favorite will I be? Who's girl will I be? I'm your girl and you love me with a love I have never had to question or doubt. I am so fortunate and blessed to have you and your deep love in my life.
I'm going to be so sad and so lonely when you go, but it will pass as our wonderful memories together fill those gaping wounds of pain that your absence will leave in my heart. I have so many memories to cherish and to remember. You have made me a better person and I know that you would be telling me (if it weren't you I was dying to hold onto), that I need to let you go and let you be happy and free and full again. You'd get on to me a little bit about my selfishness that is holding onto you. I'd shake my head and cry and know that you are right and I'd let you go.
Gran'ma, thanks for loving me so selflessly. Thanks for not being afraid to dream with me. Thanks for praying with me at night before we'd giggle until we slumbered. Thanks for walking with me through the forest and for giving me space to play when I needed it. Thanks for supporting me completely in everything I did even without words. Thanks for always having time for me and for giving me your undivided attention as we played dominoes and played make believe and pressed flowers and did life together. Thanks for knowing me better than I know myself and for being so aware of my every thought. Thanks for loving me with a love that seems, right now, to be irreplaceable.
Yes, I'm terrified, but just as I have been blessed to have you in my life, I am blessed to have such a big and loving family surrounding me. I won't be alone. I will be loved. I will be known. I just have to be brave enough to let others know me the way you know me.
So, Gram, with all of my heart and with all of my love and with rivers of tears, I want you to know that I am letting you go. Please don't hold on for me. I am going to be okay and I am so thankful that I have had someone in my life who makes saying goodbye so hopelessly impossible! I love you so much! I know you know that! You are my heart and my soul and I am forever grateful for the love you gave me and for the person you helped make me.
Go hug Pappy and tell him that I still miss him each day. I love you with all of me!
Your Girl, Jamethy Jomathy